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Biomedical subjects

A Martini

Publications and source records attributed to A Martini.

At least 343 records · Page 19Linked to original sources
PubMed1982

IgA-containing plasma cells in the intestinal mucosa of children with selective IgA deficiency.

In 8 children with selective IgA deficiency (serum IgA less than 5 mg/dl, secretory IgA less than 0.5 mg/dl in unstimulated saliva) immunofluorescent staining of intestinal biopsy specimens revealed the presence of IgA-containing plasma cells. This finding supports the hypothesis that in the intestinal mucosa of patients with IgA deficiency B lymphocytes undergo "sterile" differentiation into IgA-containing plasma cells probably incapable of secreting the IgA synthesized.

B-Lymphocytes↗
PubMed1982

Hemodynamic effects of ceruletide administered intravenously to coronaropathic patients.

The possible hemodynamic effects of ceruletide, administered intravenously at the dose of 1 ng/kg b.w., were studied in 9 coronaropathic patients submitted to cardiac catheterization. Ceruletide did not induce any modification of hemodynamic parameters. The only observed effect was a slight (3.7%) but statistically significant reduction of O2 saturation in the pulmonary artery.

Adult↗
PubMed1981

Effects of caroxazone, a reversible monoamine oxidase inhibitor, on the pressor response to intravenous tyramine in man.

1 Caroxazone is a new antidepressant drug with reversible MAO-inhibitory activity. 2 The pressor effect of intravenously injected tyramine has been evaluated in six male healthy volunteers before, during oral treatment with caroxazone 200 mg three times daily and at different time intervals after discontinuation of treatment. 3 Caroxazone produces a moderate tyramine supersensitivity. 4 The reversibility of MAO-inhibition produced by caroxazone is clearly reflected by the time-course of tyramine supersensitivity. In fact, tyramine potentiation does not accumulate with caroxazone cumulative dose, while it is correlated to drug plasma levels and disappears rapidly (half-life 1.5 days) upon discontinuation of treatment. 5 caroxazone seems to be safer and more manageable than all other clinically available MAO-inhibitors which produce irreversible inactivation of MAO.

Adult↗
PubMed1981

Effects of caroxazone, a reversible monoamine oxidase inhibitor, on the pressor response to oral tyramine in man.

1 A double-blind, placebo-controlled study was carried out in order to investigate the effects of caroxazone, a new antidepressant drug endowed with a reversible short-lasting MAO-inhibitory activity in man, on the blood pressure response to tyramine administered by the oral route. 2 The study was carried out in 9 healthy volunteers who were randomly assigned to treatment with caroxazone 200 mg three times daily (7 subjects) or with indistinguishable placebo (2 subjects). 3 The sensitivity to tyramine was assessed in each subject both before and after the 7-9 days of treatment. 4. While placebo did not modify the pressor response to tyramine, the threshold dose of tyramine which induced a rise in systolic blood pressure was lowered by about four-fold in 6 out of the 7 subjects treated with caroxazone. In the seventh subject the observed potentiation of peroral tyramine was not quantitatively evaluable. 5 Challenges performed in three subjects after discontinuation of treatment with caroxazone show that the effects of the compound are short-lasting, since the sensitivity to tyramine seems to regain the baseline value within 1-2 days. 6 Even if caroxazone potentiates peroral tyramine to a relatively low degree, a tyramine poor diet is recommended for patients during caroxazone treatment. 7 The reversibility of the MAO-inhibitory action of caroxazone is confirmed by the rapid return to normal values in the response to tyramine after discontinuation of treatment. This property of caroxazone would allow patients to return to a free diet in much less time than the safety limit of 2 weeks recommended for the currently used irreversible MAO-inhibitors.

Adult↗
PubMed1981

Goodpasture's syndrome in a child: natural history and effect of treatment.

An 8-year-old girl with microhematuria of recent onset developed a picture of pulmonary hemosiderosis in the space of 2 months. Some months later while pulmonary involvement was improving severe extracapillary glomerulonephritis developed. Circulating anti-glomerular basement membrane antibody was detected and linear deposition of IgG along glomerular basement membrane was observed. A diagnosis of Goodpasture's syndrome was made and treatment was started with prednisone, cyclophosphamide and periodic plasmapheresis with complete progressive disappearance of circulating anti-glomerular basement membrane antibody. After suspension of plasmapheresis despite immunosuppressive therapy and lack of evidence for circulating anti-glomerular basement membrane antibody, the child went into terminal renal failure. The natural history of the disease in this case and the results of treatment are discussed. To our knowledge this is the first case of Goodpasture's syndrome reported in childhood with demonstration of the presence of anti-glomerular basement membrane antibody.

Anti-Glomerular Basement Membrane Disease↗
PubMed1981

Pharmacodynamic model describing the growth of a mammary carcinoma in the mouse under the influence of adriamycin treatment.

The chemotherapeutic effects of different doses of adriamycin in (C3H x 020)F1 mice bearing mammary carcinoma have been investigated and a model of the growth of neoplastic cells under the influence of treatment is described. An estimate of cell kill and of the fraction of cells surviving after treatment is given by the efficacy constant K, which is a function of the dose level of the drug. The therapeutic value of each treatment is, however, also related to the degree of toxicity which in our model is expressed by the probability of death for each dose level.

Animals↗
PubMed1981

Opiates act centrally on GH and PRL release.

This study was conducted in order to further understand whether the effect of opiates on growth hormone and prolactin release was exerted centrally or at least in part peripherally. Male rats were treated with morphine-HCl after pretreatment with saline with either the opiate antagonist naloxone-HCl or the quaternary derivative naloxone methyl bromide (Naloxone-Br), the latter of which does not cross the blood brain barrier. Morphine-HCl elicited a clear cut increase in prolactin and growth hormone release after pretreatment with naloxone-Br, but not after pretreatment with naloxone-HCl. Naloxone-Br, however, was able to inhibit the effect of morphine when administered directly in the brain ventricles. To further confirm these results, we administered the quaternary derivative morphine-methyl-iodide (morphine-I), which unlike morphine-HCl, does not cross the blood brain barrier. Morphine-I was ineffective in eliciting growth hormone and prolactin release when administered peripherally, but was effective when administered intraventricularly.

Animals↗