Biomedical subjects

M M Mariscalco

Publications and source records attributed to M M Mariscalco.

21 records · Page 2Linked to original sources

PubMed1990

Effects of serum and endotoxin in experimental lung injury.

Lipopolysaccharide (LPS) is in large part responsible for the lung injury that occurs in the sepsis syndrome. Recent work has shown the ability of LPS alone to induce injury in endothelial monolayers, though the LPS effect is enhanced in the presence of serum. We previously demonstrated that low-dose LPS (50 ng/mL) can lead to lung injury in an isolated perfused rabbit lung model. To examine the effect of serum on LPS-induced injury rabbit lungs were perfused with increasing doses of rabbit serum in the presence and absence of LPS. There was no increase in total weight gained by the lung,Qf, with either 5% serum, 10% serum, or 10% serum with LPS. However vascular permeability as measured by hydraulic conductance was increased with increasing doses of serum. This effect was not enhanced by the addition of LPS. These results provide evidence that serum alone may cause lung injury, perhaps through the activation of complement or other mediators.

Animals↗

PubMed1990

Back pain with cardiovascular collapse in a pediatric emergency department patient.

Severe back pain in the pediatric patient is an infrequent complaint. The following case report illustrates the disastrous outcome for this patient with back pain secondary to aortic dissection. The most common predisposing disease process is hypertension, which exposes the aortic wall to high pressures and flows. Just as in the adult patient, the possibility of aortic dissection should be included in the differential diagnosis of acute onset of severe back pain with preexisting hypertension in the pediatric patient. A high index of suspicion is warranted.

Adolescent↗

PubMed1988

Recognition of an endothelial determinant for CD 18-dependent human neutrophil adherence and transendothelial migration.

Human neutrophil (PMN) attachment to human umbilical vein endothelial cells (HUVEC) was evaluated in vitro using two MAbs, R6-5-D6 and RR1/1, that recognize intercellular adhesion molecule-1 (ICAM-1), and one MAb, TS1/18, that recognizes CD18. Pretreatment of the HUVEC with anti-ICAM-1 MAbs produced greater than 50% inhibition of attachment to HUVEC, and IL-1 (0.5 U/ml)- or lipopolysaccharide (LPS) (10 ng/ml)-stimulated HUVEC, and greater than 99% inhibition of f-Met-Leu-Phe (0.5 nM) enhanced adherence. Anti-ICAM-1 MAbs also inhibited by greater than 85% the transendothelial migration induced by 4-h IL-1 (0.5 U/ml) and LPS (10 ng/ml) activation of the HUVEC. That these effects involved a CD18-dependent mechanism is supported by the following results: pretreatment of PMN with TS1/18 produced the same degree of inhibition of attachment and migration as seen with R6-5-D6. In addition, the use of both MAbs together did not further increase the inhibition of cell attachment to stimulated HUVEC. The attachment of PMN from patients with CD18 deficiency to stimulated HUVEC was not reduced by R6-5-D6, and both R6-5-D6 and TS1/18 revealed the same time course for appearance and disappearance of an adherence component on stimulated HUVEC not blocked by either MAb. These results demonstrate that attachment and transendothelial migration of PMN in vitro depend substantially on both CD18 on the PMN and ICAM-1 on the endothelial cell.

Antibodies, Monoclonal↗