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Biomedical subjects

M Barbero

Publications and source records attributed to M Barbero.

42 records · Page 3Linked to original sources
PubMed1985

The concentrations of 6-keto-PGF1 alpha and TXB2 in plasma samples from patients with benign and malignant tumours of the breast.

Peripheral plasma concentrations of 6-keto-PGF1 alpha and TXB2 were measured in patients with benign and malignant tumours of the breast, in patients with non-gynecological diseases, and in healthy female controls. The values were significantly higher in female patients with malignant tumours of the breast than in healthy controls (146 +/- 28 vs 13 +/- 2.5 pg/ml for 6-keto-PGF1 alpha p less than 0.01 and 78 +/- 17 vs 11 +/- 2 pg/ml for TXB2, p less than 0.01). Benign tumours of the breast were also associated with significantly raised plasma levels of 6-keto-PGF1 alpha and TXB2 compared to normal controls (52 +/- 5 vs 13 +/- 2.5 pg/ml for 6-keto-PGF1 alpha, p less than 0.01 and 26 +/- 5 vs 11 +/- 2 pg/ml for TXB2, p less than 0.05). The high levels of 6-keto-PGF1 alpha and TXB2 were not found to be correlated with clinical and histopathological data. The surgical removal of the primary tumour has apparently no effect on the plasma concentrations of 6-keto-PGF1 alpha and TXB2 over a follow-up period of 9 days after operation. The lack of alterations in the ratio of TXB2:6-keto-PGF1 alpha in the cancer patients and other subjects studied before and after surgery is indicative of the regulatory power of metabolic systems to preserve the homeostatic balance.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Production of prostacyclin (PGI2) and thromboxane A2 (TXA2) by vessels draining and not-draining benign and malignant tumours of the breast.

The production of PGI2 (determined by bioassay) and TXB2 (determined by radioimmunoassay) was studied in the supernatant solutions obtained after incubation of vessel rings prepared from veins draining and not draining benign and malignant tumours of the breast. A significant increase (p less than 0.01) was found in the production of PGI2 by vessels draining the malignant tumours as compared to those not draining such tumours or vessels draining benign tumours. The changes in PGI2, and the tendency for TXB2 to be higher in vessels draining malignant tumours, were in the same direction so that they balanced out when the ratio PGI2/TXB2 was calculated: in consequence no significant changes in this ratio were found in malignant tumours as compared to the benign. A significant difference (p less than 0.01) was observed in the ratios of vessels draining tumours:vessels not draining tumours between malignant and benign tumours in relation to the production of PGI2. The present data demonstrate that the production of PGI2 by vessels draining malignant tumours of the breast is different to that obtained with vessels from patients with benign tumours, although the mechanism responsible for this difference is not known.

Adult↗
PubMed1984

Production of prostacyclin, 6-keto-PGF1 alpha and thromboxane B2 by incubated samples of umbilical vessels: a comparison of methods for expressing the results on dry weight, wet weight, protein or DNA bases.

The production of PGI2 (determined by bioassay), and of 6-keto-PGF1 alpha and TXB2 (determined by radioimmunoassay) by samples of human umbilical vessels have been measured. The results have been calculated on four bases: dry weight, wet weight, protein and DNA. There was a higher production of PGI2 and 6-keto-PGF1 alpha by umbilical veins than by umbilical arteries; no significant difference in TXB2 production was observed between umbilical veins and arteries. The ratio of 6-keto-PGF1 alpha: TXB2 production was about 100 for the samples of veins and about 40 for the samples of arteries. The best methods of expressing the results were on the bases of protein and DNA, the latter basis being marginally the best. The least satisfactory method for expressing the results was that based on dry weight. The physiological and practical implications of the results are discussed.

6-Ketoprostaglandin F1 alpha↗