Biomedical subjects
S Alessi
Publications and source records attributed to S Alessi.
[Neuroleptic-induced dysphoric response in non-schizophrenic patients].
In 50 psychiatric inpatients treated with neuroleptics we observed neuroleptic-induced dysphoria in 4% and neuroleptic-induced akathisia in 18% of the cases. In our sample there was no schizophrenics among dysphoric responders. We discuss the implication of the findings and the relationship between dysphoric response and subjective phenomena of akathisia.
Brain tumours in south Brazil: a retrospective study of 438 cases.
All brain tumours diagnosed since 1967 in a University Hospital in the Southern region of Brazil were reviewed and clinical information concerning age, sex, symptoms and evolution were analysed. 88.1% of tumours were primary neoplasms and the rest secondary deposits. There was a male predominance and the second and fifth decades of life were the most affected. The main presenting symptoms were headache, vomiting, hemiparesis, loss of vision and epilepsy. The commonest tumour was of astrocytic origin (36.3%) amongst which the malignant ones, including glioblastoma multiforme, predominated. These tumours were frequent in the cerebral hemispheres (31.3%), particularly in the frontal lobes. The time of evolution from the beginning of the clinical manifestations until the first hospital admission was also studied. The authors discuss the clinical and pathological observations in relation to other large series analysed in the literature.
Differential sensitivity of T suppressor cell expression to inhibition by histamine type 2 receptor antagonists.
The ability of the histamine type 2 (H2) receptor antagonists cimetidine and oxmetidine to inhibit the immune suppression mediated by different types of murine T suppressor cells has been evaluated. Both compounds at doses as low as 1 mg/kg administered as a per os (p.o.) twice a day (b.i.d.) regimen abrogated the expression of dinitrobenzene sulfonic acid-induced, Lyt-2+, T suppressor cells and stimulated contact sensitivity to dinitrofluorobenzene in adoptive transfer experiments. Comparable inhibition of Lyt-1+, T suppressor cell activity induced by UV irradiation required higher doses of cimetidine and oxmetidine (200 and 25 mg/kg; p.o., b.i.d., respectively). In contrast, the T suppressor cell-mediated unresponsiveness induced by inoculation with a high dose of sheep red blood cells was refractory to treatment in vivo with either cimetidine or oxmetidine regardless of the dose. These results indicate that T suppressor cell populations differ markedly in their susceptibility to modulation by H2 antagonists. The histamine type 1 (H1) receptor antagonist diphenhydramine, had no effect on suppressor cell activity in any of these systems, indicating that modulation of suppressor cell activity is mediated through an H2 receptor interaction.
Inhibition of T suppressor cell expression by histamine type 2 (H2) receptor antagonists.
The effect of histamine type 2 (H2) receptor antagonists, cimetidine and ranitidine, on the induction and expression of hapten-specific suppressor T cells was studied. The activity of DNBSO3 -induced suppressor cells was evaluated after adoptive transfer to naive syngeneic recipients. Treatment with cimetidine or ranitidine markedly inhibited suppressor T cell activity in a dose-related manner and enhanced the contact sensitivity response to DNFB. Both H2 antagonists were effective in inhibiting the expression and, to a lesser extent, the induction of suppressor T cells. In contrast, norburimamide , a non-H2 antagonist structurally related to cimetidine, was inactive. The relevance of these findings to the clinical observation of cimetidine-induced reversal of acquired tolerance to dinitrochlorobenzene in anergic patients is discussed.
Inhibition of carrageenan-induced inflammation by urethan anesthesia in adrenalectomized and sham-operated rats.
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Stimulation of contact sensitivity to oxazolone by disodium cromoglycate.
The subcutaneous administration of 0.01-10 mg/kg of the antiallergic agent disodium cromoglycate on day 0 30 min prior to sensitization of C57Bl/6 male mice with 5% 2-phenyl-4-ethoxy-methylene oxazolone proved to cause a significant stimulation of the low-grade volume response as measured plethysmographically in 24 h after challenge. The investigation of the mechanism favors the conclusion that histamine release is involved in the action of disodium cromoglycate as judged by the ability of the antihistaminics chlorpheniramine and metiamide to inhibit the disodium cromoglycate action and by the inhibitory effect of polymyxin B induced depletion of histamine.