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E Bastida

Publications and source records attributed to E Bastida.

76 records · Page 5Linked to original sources

Interleukin-1 increases tumor cell adhesion to endothelial cells through an RGD dependent mechanism: in vitro and in vivo studies.

The effects of human recombinant interleukin-1 alpha and beta (rIL-1 alpha; rIL-1 beta) on the adhesion of human A549 lung carcinoma cells and M6 melanoma cells (TC) to human endothelial cells (HECs) in vitro were studied, and on TC/lung entrapment in vivo. In vitro, there was a significant increase in TC/HEC adhesion to HECs pretreated for 4 h with rIL-1 alpha or rIL-1 beta. The effects of rIL-1 alpha and beta on TC/HEC adhesion were time dependent and reached a plateau within 4-6 h. TC/HEC adhesion was not blocked when measured in the presence of antibodies to either fibronectin, glycoprotein IIb/IIIa, anti-ICAM, or anti-LFA. However, enhanced TC/HEC adhesion was completely blocked in the presence of the peptide, GRGDS. In vivo, pretreatment of nude mice for 4 h with rIL-1 alpha (given i.p. before i.v. injection of TCs) enhanced TC retention in the lung 24 h later. Our data demonstrate that IL-1 enhances TC adhesion to the vascular surface both in vitro and in vivo, suggesting that IL-1 can facilitate the metastatic process.

Animals↗

Platelet adhesion to exposed endothelial cell extracellular matrixes is influenced by the method of preparation.

The relative thrombogenicity of extracellular matrixes (ECMs) produced by cultured human umbilical endothelial cells (ECs) was studied under flow conditions. ECMs were prepared using a number of physical and chemical methods, and their reactivity toward platelets was morphometrically evaluated. von Willebrand factor (vWF), fibronectin (FN), and 13-hydroxy-9-cis,11-trans-octadecadienoic acid (13-HODE) were also determined. We found that platelet adhesion to ECMs differed significantly, both quantitatively and qualitatively, with the method of ECM preparation. Mechanically prepared ECM exposed a less thrombogenic surface compared with ECM prepared by chemical methods (platelet-covered surface of 20% and 50%, respectively). Evaluation of the ECM components vWF, FN, and 13-HODE showed significant changes, both in their concentrations and distribution patterns, depending on the method of ECM preparation. The decrease measured in the levels of ECM-associated vWF (from 108 to 9.2 ng/10(4) cells) and the minor changes observed in the distribution pattern of subendothelial FN did not appear to be sufficient to explain the altered platelet adhesion observed in our model. This suggests that the amount of 13-HODE probably associated to the remaining ECs present in the mechanically exposed ECM could be one factor that specifically contributed to the nonthrombogenic state of these preparations. We conclude that the degree of ECM reactivity toward platelets is dependent on the method of ECM preparation and that this is related to the removal of specific EC/ECM components that modulate their thromboresistant/thrombogenic properties. This fact should be taken into account when ECMs produced by cultured ECs are used in platelet adhesion studies.

Antithrombins↗

Regulation of tumor cell adhesion by intracellular 13-HODE: 15-HETE ratio.

We performed studies to determine whether tumor cells (TCs) produce 13-hydroxyoctadecadienoic acid (13-HODE) and 15-hydroxyeicosatetraenoic acid (15-HETE), and to determine the relationship between TC and endothelial cell (EC) 13-HODE and 15-HETE synthesis, and TC adhesion to ECs and their underlying extracellular matrix (ECM). We measured (1) the amounts and ratios of 13-HODE: 15-HETE in three different human TC lines and in three different murine TC lines under basal and stimulated conditions; and (2) the relationship between 13-HODE synthesis and cAMP levels in TCs and ECs. Under basal conditions, TCs produced both 13-HODE and 15-HETE, the intracellular ratios of which correlated with TC adhesivity. Stimulation of the TCs with the chemotactic tripeptide, N-formyl-methionyl-leucyl-phenylalanine, decreased 13-HODE synthesis, and increased 15-HETE synthesis and TC adhesion to ECs and to their ECM. Alternatively, enhancing 13-HODE synthesis in either TCs or ECs (by elevating the resting levels of intracellular cAMP) was associated with decreased TC adhesion to ECs and ECM. These results suggest that intracellular 13-HODE: 15-HETE ratio in TCs regulates TC adhesivity, and that an alteration in 13-HODE: 15-HETE ratio will markedly influence TC adhesion.

Animals↗

[Myocardial revascularization: isoflurane and halothane. Our experience].

The use of isofluorane in coronary patients has been questioned due to the coronary steal syndrome that this agent is said to produce with changes in the myocardial lactate extraction, ST segment changes or T wave inversion. Three hundred fifty nine patients underwent coronary revascularization were studied. The anaesthesia was carried out with halothane (146 patients) or isofluorane (213 patients) as volatile agents of a balanced anesthetic technique based on high doses of narcotics. We found no correlation between the use of isofluorane and ST changes or T wave inversion. The appearance of myocardial infarction between the 2 groups was also no statistically difference (p = 0.61).

Female↗