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Biomedical subjects

A Moldovan

Publications and source records attributed to A Moldovan.

16 recordsLinked to original sources
PubMedDate not supplied

Activation of carbonic anhydrase by beta-adrenergic agonists and inhibition by beta-adrenergic blockers.

Knowing the in vitro and in vivo gastric secretory effects of beta-adrenergic agonists and antagonists, as well as the role of carbonic anhydrase in the gastric HCl production, we investigated the effect of some beta-adrenoceptor agonists (isoprenaline and orciprenaline) and antagonists (propranolol, timolol, atenolol, pindolol, acebutolol, metoprolol, exoxprenolol) on the purified, human red blood cell and gastric mucosa carbonic anhydrase. All the drugs were added to enzymatic preparations in a concentration range of 10(-7)-10(-3) M, the enzymatic activity being determined according to Maren's micro-method. Dose-response relationships were plotted for each drug. The activating effect of the beta-adrenergic agonists isoprenaline and orciprenaline on all the three species of carbonic anhydrase was dose-dependent, maximum effect being reached at 10(-3) M, when a highly significant (p less than 0.001) enzymatic activation was achieved. Beta-adrenergic blocking drugs decreased significantly the activity of carbonic anhydrase, thus, the activity of purified enzyme decreased with propranolol depending on the dose from 2140 +/- 68 to 1060 +/- 82 I.U. (p less than 0.001), that of red blood cell enzyme from 3340 +/- 280 to 1050 +/- 180 I.U. (p less than 0.001) and that of gastric mucosa enzyme from 2.1 +/- 0.2 to 1.1 +/- 0.1 E.U./mg bioptic sample. They also antagonized dose-dependently the activating effect of beta-adrenergic agonists on the enzyme. The results suggest that carbonic anhydrase might be one of the sites of beta-adrenoceptors, further studies using specific radioligands being necessary to elucidate whether these effects represent the interaction of these drugs with their specific receptor or if they are unspecific pharmacologic effects.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Action of aflatoxin B1 on pregnant rats.

The hepatotoxic effect of aflatoxin B1 on pregnant rats was studied by injecting the animals in the first 14 days of pregnancy with doses equivalent ot 1/1,000 ppm; the rats were killed at the end of pregnancy. Liver lesions such as clear intumescence, granular dystrophy, Kupffer cell hyperplasia, pycnosis and atypical mitoses were shown; concomitantly regeneration phenomena were expressed by an increased incidence of binucleated cells and mitosis. Fertility decreased after aflatoxin and embryonary resorptions, malformations and developmental retardations occurred.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

The toxic and teratogenic effect of aflatoxin B1 on the chick embryo development.

The embryotoxic and teratogenic effect of aflatoxin B1 was tested on the chick embryo. Aflatoxin B1 was injected into the embryonic area in doses of 1/100 ppm and 1/500 ppm in the 96th h of incubation. Aflatoxin B1 toxicity caused a rise in the mortality rate from 6.6% (controls) to 35% in the chicken injected with 1/100 ppm aflatoxin B1 and to 26% in the lot given 1/500 ppm. Several malformations were also noticed: spina bifida, anophthalmia, maxillary retrognathism, distorted legs and evisceration; the group receiving 1/100 ppm aflatoxin B1 also showed bone development retardation of the wing, leg, maxilla and mandible.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

[Pulmonary hamartomas--apropos 3 clinical cases].

The study starts with presentation of present day knowledge of the disease. Its features are predominantly X-ray images consisting mainly in a round or ovular, usually solitary formation ("coin lesion"). The clinical expression of the disease is usually very discrete, the general state unmodified. The X-ray evidencing follows a routine examination. 3 cases of personal observations are presented. All cases were solved by surgery, by removal of tumour. Etiology is fixed by histological examination of surgery specimen. All aspects risen by the differential diagnosis are largely discussed focusing on lung granuloma (e.g. tuberculoma) lung abscess, limited pneumonia, lipoid pneumonia a.o. Hamartomas are of mesenchymal origin, they are not considered just as tumours but very similar to "tumour-like", without invasive evolution.

Adult↗
PubMedDate not supplied

Insulin resistance: the link between impaired glucose tolerance, body mass index and plasma lipids.

Body mass index defined as weight (Kg)/height (cm2) and plasma lipids (total lipids-TL, triglycerides-TG and cholesterol-CH) were determined in 131 patients (61 males and 70 females aged between 21 and 63 years) with impaired glucose tolerance (IGT) defined according to WHO criteria. Blood glucose (BG) values and plasma insulin (PI) levels (radioimmunological assay) were determined during 2 hours OGTT with samples obtained before and after 1 h and 2 h after the intake of 75 g glucose. The sum of blood glucose and plasma insulin levels (0 + 1h + 2h) were compared in each of the following 5 groups of subjects: A--25 cases with IGT but without obesity (BMI: 23.2 +/- 2.6) and hyperlipidaemia (PL: 627 +/- 112; TG: 102 +/- 109 and CH: 208 +/- 35 mg/dl); B--35 cases with IGT and obesity (BMI: 31.2 +/- 2.6) but without hyperlipidaemia (PL: 807 +/- 109; TG: 136 +/- 31 and CH: 254 +/- 41 mg/dl); C--23 cases with IGT and hyperlipidaemia (PL: 1013 +/- 217; TG: 214 +/- 85 and CH: 311 +/- 52 mg/dl) but without obesity (BMI: 25.4 +/- 1.9); D--48 cases with IGT and both obesity (BMI: 30.9 +/- 2.8) and hyperlipidaemia (PL: 1457 +/- 155; TG: 597 +/- 188 and CH: 483 +/- 184 mg/dl); a control group of 49 cases without IGT, obesity (BMI: 26.2 +/- 1.9) or hyperlipidaemia (PL: 726 +/- 99 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗