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Biomedical subjects
M Becht
Publications and source records attributed to M Becht.
[Cutaneous leishmaniasis in 49 patients in The Netherlands].
In a retrospective study the data concerning 49 patients with cutaneous leishmaniasis were analysed. The group included 39 patients seen in Amsterdam in the period 1979-1988 in the Royal Institute for the Tropics and the University Medical Centre and 10 patients seen in the University Hospital of Leiden in the period 1970-1982. Mediterranean countries, especially Spain, were important sources of infection. In 26 patients, one skin lesion was found. All but one of the patients had (papulo)nodules, nodules with central scab formation and/or ulcerative skin lesions. In most cases the lesions were localized on the face and extremities, one patient had a mucosal lesion of the nose, three had sporotrichoid extension and six, lymphadenitis. For demonstration of the parasite, aspiration, smear, biopsy and culture were used with varying frequencies. The biopsy and culture methods contributed most to the diagnosis. The treatment in 22 patients consisted in parenteral administration of sodium stibogluconate while 13 received primary cryotherapy. In addition, four patients were subjected to cryotherapy because of a recurrence after, or side effects of the treatment with sodium stibogluconate. In three patients, spontaneous healing was awaited. Owing to incomplete follow-up, the ultimate condition was not known of all patients; the skin lesions treated with cryotherapy all healed. In case of nodular and ulcerative skin lesions in a person who has lived in the (sub)tropics, cutaneous leishmaniasis should be considered; the geographical anamnesis is of great importance in this respect.
Adult↗
The inhibitory effect of HOE 731 in isolated rabbit gastric glands.
HOE 731, a substituted thienoimidazole derivative, was studied on [14C] aminopyrine uptake and oxygen consumption in isolated rabbit gastric glands. HOE 731 caused a concentration-dependent inhibition of [14C]aminopyrine uptake during histamine and dbcAMP stimulation. The inhibition during dbcAMP stimulation was in accordance with its proton-pump inhibiting properties, which has already been reported. (Herling et al., Gastroenterology 96: A206, 1989). IC50 values were during histamine stimulation 0.8 +/- 0.3 microM and during dbcAMP stimulation 1.3 +/- 0.4 microM. The inhibition was reversible after addition of dithioerythritol and was of a non-competitive type. Omeprazole caused similar inhibitory effects in the same concentration-range. During time-course studies in glands, the inhibitory effect on [14C]aminopyrine uptake of 0.1 microM HOE 731 already appeared after 10 min of incubation but decreased with increasing incubation time, while 0.1 microM omeprazole caused an unchanged inhibition which started after 30 min of incubation. The concentration of 3 microM of HOE 731 and omeprazole caused a comparable constant inhibition. After pre-incubation for 135 min under basal conditions with subsequent stimulation of the glands with dbcAMP, the inhibitory effect of 10 microM HOE 731 also decreased in contrast to omeprazole. During stimulation for 4 hr, the inhibition of both compounds remained constant. In oxygen consumption studies HOE 731, at 100 microM, caused a strong inhibition down to basal values. This inhibitory effect could be prevented totally when 10 mM imidazole was added to neutralize the acidic compartment of the parietal cell during stimulation. It is concluded that HOE 731 needs acid-activation like omeprazole to inhibit the proton pump, but probably due to its chemical differences (stability, pH for conversion of HOE 731 to its active form) it shows a different inhibitory profile (faster transformation into its active moiety with faster onset of a partially reversible inhibition) as compared to omeprazole.
Adenosine Monophosphate↗
Inhibition of 14C-aminopyrine accumulation in isolated rabbit gastric glands by the H2-receptor antagonist HOE 760 (TZU-0460).
Acid secretion in isolated rabbit gastric glands was measured by means of the 14C-aminopyrine accumulation technique. Hoe 760 (TZU-0460) and Hoe 062, the desacetylated compound of Hoe 760, caused a concentration-dependent reduction of histamine (100 microM) induced aminopyrine-accumulation. The IC50-values were 3.16 +/- 0.84 microM (n = 5) and 1.58 +/- 0.6 microM (n = 6) for Hoe 760 and Hoe 062, respectively. In comparison an IC50 of 9.0 +/- 0.72 microM (n = 6) was obtained for cimetidine and 3.3 +/- 1.4 microM (n = 5) for ranitidine. The IC50-values of ranitidine, Hoe 760 and Hoe 062 were significantly different (p less than 0.05) from cimetidine. The addition of increasing concentrations of Hoe 760 to the histamine concentration-response curve caused a parallel rightward shift. The transformation of these concentration-response curves according to Arunlakshana and Schild indicated that this inhibition was caused by a competitive antagonism of the histamine receptor on the parietal cell. In agreement with these findings the dbc-AMP stimulated aminopyrine accumulation remained unaffected by the H2-receptor antagonists.
Aminopyrine↗