Biomedical subjects
Publications and source records attributed to L Vicentini.
1 Muscimol, a gamma-aminobutyric acid (GABA) receptor agonist, when injected intraventricularly antagonizes the antinociceptive effect of morphine given either subcutaneously or intraventricularly. The antagonistic effect of muscimol on morphine analgesia appears to be linearly related. 2 This finding provides support for the view that a GABA-ergic system is involved in morphine analgesia.
Mazindol, a new anorexigenic agent which possesses a different chemical structure from phenylethylamine derivatives such as amphetamine, causes anorexia along with increases in locomotor activity and body temperature. Mazindol also induces stereotyped behaviour and, if injected into rats with unilateral nigro-striatal lesions, causes turning towards the lesioned side. Mazindol-induced anorexia is antagonized by pretreatment with alpha-methyl-p-tyrosine or pimozide. Pimozide pretreatment prevents the rotation induced by Mazindol in rats with unilateral nigro-striatal lesions. The involvement of dopamine in the mechanism whereby Mazindol elicits anorexia and turning behaviour is discussed.
1 Mazindol is a new anorexigenic agent which possesses a different chemical structure from that of phenylethylamines, but shows a pharmacological profile similar to that of (+)-amphetamine. 2 Mazindol neither altered whole brain monoamine levels (noradrenaline (NA), dopamine, 5-hydroxytryptamine (5-HT)) nor changed NA levels in the hypothalamus or dopamine levels in the caudate nucleus. 3 Mazindol enhanced dopamine turnover rate in the caudate nucleus, as shown by the increased rate of dopamine decline after blockade of catecholamine synthesis by alpha-methyl-p-tyrosine and decreased the conversion index of (3H)-tyrosine into brain NA. 4 Mazindol administration did not modify pargyline-induced decline of 5-hydroxyindoleacetic acid suggesting that 5-HT turnover is not altered by this drug.
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Systemic administration of parachlorophenylalanine (PCPA, 100 mg/kg sc on alternate days X two times), a blocker of serotonin (5-HT) synthesis, considerably decreased brain 5-HT and plasma prolactin (PRL) levels in young male rats. Intraventricular (IVT) administration of 5,7-dihydroxytryptamine (5,7-DHT, 200 mug/20 mul), a neurotoxic drug which destroys 5-HT nerve terminals, induced, 3, 12, and 30 days after treatment, a marked depletion of brain 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) and considerably reduced plasma PRL levels at each time interval. Feeding of rat for up to 4 days with a tryptophan (TP)-deficient diet, caused a depletion of brain 5-HT and 5-HIAA contents and did not modify plasma PRL levels. Addition of TP (2 g/kg of diet) to the TP-deficient diet resulted in increased brain 5-HT and 5-HIAA contents and significantly increased PRL levels. These data provide evidence for the role of the 5-HT system in the maintenance of tonic PRL secretion.
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Hereditary periodic fever syndromes are a group of systemic disorders characterized by recurrent attacks of systemic inflammation (autoinflammation) without infectious or autoimmune cause. The hyper-IgD syndrome (HIDS) is a rare autosomal recessive inflammatory disorder characterized by recurrent fever, increased serum IgD (normal value < 100 U/ml) and generalized inflammation (lymphadenopathy, arthralgias/arthritis, abdominal complaints, skin rash, and headache). The attacks persist during the entire life although frequency and severity tend to diminish with age. HIDS is caused by specific mutations in the gene encoding mevalonate kinase, resulting in depressed enzymatic activity. At present the therapy for the syndrome is only supportive. Other than HIDS, other hereditary systemic inflammatory disorders have been described: the Familial Mediterranean Fever, the tumour necrosis factor receptor associated periodic syndrome (TRAPS), a disease related to the mutations of one of the TNF receptors, the Familial Cold Urticaria and the Muckle-Wells syndrome. The differential diagnosis with other causes of periodic fever is crucial for assessing appropriate management and treatment.
Two cases of primary large B-cell non-Hodgkin's lymphoma are described. Both cases had typical symptoms: a sudden growth of thyroid in these female patients at their sixth decade of life. The differential diagnosis between undifferentiated carcinoma and lymphoma of the thyroid, uncertain with clinical and ultrasound examination, was defined by a fine needle biopsy (FNAB). Patients underwent a radical resection which permitted a correct cancer staging even in the presence of laterocervical lymph nodes swelling. Histological examination of the surgical specimen confirmed the presence of a large B-cell non-Hodgkin's lymphoma while the immunophenotypical analysis detected the expression of the common leukocytic antigen and B-correlated antigens CD20, CD74, CDW75 and CD79A. In both cases chemotherapy and radiotherapy were carried out.
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Ultrasound is mandatory in the follow up of patients surgically treated for benign thyroid diseases. In this study the Authors have examined 87 patients who underwent different surgical treatments for goiter over 40 years. Ultrasound allowed a more accurate study of residual thyroid, particularly evaluating thyroid tissue morphology in symptomatic patients (43.6%) and detecting many recurrences in asymptomatic patients (37.3%). This study also confirms the advantage of a more extensive surgery to reduce recurrences without increasing complications.
The contribution of beta 2-agonist treatment per se and the effect of beta 2-agonists plus allergen exposure was evaluated in two groups of thirteen asthmatic children being treated respectively at sea level during the period of maximal allergen exposure and at high altitude in an environment free of the offending allergens. Bronchial hyperreactivity was evaluated by standardised exercise tests before and after treatment with salbutamol controlled release tablets (4 mg). Challenges were performed at the beginning and after 2 and 4 weeks of treatment. A fourth test was performed 2 days after stopping the treatment. Children treated with salbutamol at sea level (exposure to allergen) showed baseline delta PEF of 16.9 +/- 3.4 and 13.7 +/- 4.2, 20.7 +/- 4.3, 26.0 +/- 5.1 respectively for the second, third and fourth test. Children treated at high altitude showed respectively delta PEF of 34.9 +/- 5.1, 31.1 +/- 4.9, 26.5 +/- 5.4, 27.9 +/- 5.0. These data suggest that oral salbutamol per se is not responsible for an increase in bronchial responsiveness, but eventually suggest that treatment with beta 2-agonists at the same time as continued allergen exposure may be responsible for an increase in bronchial hyperresponsiveness.