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Biomedical subjects

R A Kaslovsky

Publications and source records attributed to R A Kaslovsky.

7 recordsLinked to original sources
PubMed1997

Bronchioloalveolar carcinoma in a child with congenital cystic adenomatoid malformation.

An 11-year-old girl was evaluated for chest pain, and chest radiographic findings of multiple nodules throughout both lungs. She underwent resection of several of the lesions from her left lung, which were found at pathologic examination to be bronchioloalveolar carcinoma. Her previous medical history included incomplete resection of a type I congenital cystic adenomatoid malformation in the neonatal period. To our knowledge, this girl is the youngest reported case of bronchioloalveolar carcinoma in a nonimmunocompromised patient, and one of several in which the association of congenital cystic adenomatoid malformation and bronchioloalveolar carcinoma has been observed.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1993

Mediation of endothelial injury following neutrophil adherence to extracellular matrix.

Since polymorphonuclear leukocytes (PMN) rapidly migrate across the endothelial barrier and attach to extracellular matrix components, we tested the hypothesis that adhesion of PMN to matrix proteins can mediate endothelial injury following PMN activation. Studies were made using gelatin- and fibronectin-coated polycarbonate microporous filters (10 microns thick) on which confluent monolayers of bovine pulmonary microvessel endothelial cells were grown. PMN were layered either directly onto endothelial cells (at a ratio of 10:1) ("upright system") or onto gelatin- and fibronectin-coated filters with the endothelial monolayer grown on the underside of the filter without contact between PMN and endothelial cells ("inverted system"). PMN were activated with phorbol 12-myristate 13-acetate (PMA; 5 x 10(-9) M) in both systems. PMN activation increased endothelial permeability to 125I-labeled albumin in upright as well as inverted systems. Pretreatment of PMN with anti-CD18 monoclonal antibodies IB4 or R15.7, which inhibited PMN adherence to matrix constituents as well as to endothelial cells, prevented the permeability increase in both configurations. This effect of anti-CD18 monoclonal antibodies (mAbs) was not ascribed to a reduction in PMN activation, since PMA-induced superoxide generation was unaffected. We conclude that activation of PMN adherent to extracellular matrix proteins increases endothelial permeability to albumin and that this response is dependent on PMN adhesion to the matrix. The results support the concept that PMN-mediated increase in endothelial permeability is the result of "targeted" release of PMN products independent of whether the PMN are adherent to the extracellular matrix or the endothelium.

Animals↗
PubMed1991

Neutrophils from chronic granulomatous disease fail to increase endothelial permeability.

Studies of neutrophil-dependent endothelial injury were made using normal neutrophils (nl-PMN, i.e., normal polymorphonuclear neutrophils) and PMN obtained from a patient with X-linked chronic granulomatous disease (CGD-PMN). Layering of nl-PMN on bovine pulmonary microvessel endothelial monolayers (ratio 10:1) followed by challenge with phorbol 12-myristate 13-acetate (PMA; 5 x 10(-9) M) resulted in a 190% increase in 125I-labeled albumin permeability across the monolayers. Pretreatment of endothelial monolayers with tumor necrosis factor-alpha (TNF-alpha; 200 or 1,000 U/ml) further enhanced the increase in permeability after stimulation of nl-PMN with PMA. In contrast, challenge of CGD-PMN layered on endothelial cells with PMA did not increase permeability, and the effect was not enhanced by pretreating the endothelial cells with TNF-alpha. Nl-PMN, but not CGD-PMN, generated superoxide anion on stimulation with PMA (42.5 +/- 0.7 vs. 6.5 +/- 0.6 nM.10(6) PMN-1.h-1). PMA also induced degranulation of nl-PMN as measured by release of elastase (2.32 +/- 0.12 micrograms/10(6) PMN) and myeloperoxidase (173.8 +/- 1.9 U/10(6) PMN) into the medium, whereas release by CGD-PMN was markedly reduced (elastase release of 0.88 +/- 0.04 microgram/10(6) PMN and myeloperoxidase release of 82.6 +/- 19.4 U/10(6) PMN). The adherence response of nl-PMN and CGD-PMN to the endothelial cells after PMA stimulation was similar (79.5 +/- 11.8% nl-PMN and 64.0 +/- 1.9% CGD-PMN). Therefore, the PMN respiratory burst, with the resultant generation of oxidants and PMN-derived proteases, is required to increase endothelial permeability even in the face of increased endothelial adhesivity.

Adult↗
PubMed1990

Pulmonary edema induced by phagocytosing neutrophils. Protective effect of monoclonal antibody against phagocyte CD18 integrin.

We studied the changes in pulmonary hemodynamics and lung wet weight induced with opsonized zymosan (OZ) in isolated guinea pig lungs perfused with Ringer-albumin solution containing neutrophils (PMNs). Addition of OZ to the PMN-perfused lungs caused pulmonary vasoconstriction and weight gain; neither OZ nor PMNs added individually to the perfusate altered pulmonary vasomotor tone or wet weight. The steady gain in lung weight by 1,588 +/- 464 mg over the 45-minute study period was associated with pulmonary capillary hypertension and an increase in the capillary filtration coefficient, indicative of increased lung vascular permeability. These responses may not be due to generation of oxygen radicals, because the alterations in pulmonary hemodynamics and lung weight were not reduced by addition of superoxide dismutase, catalase, or superoxide dismutase plus catalase. We examined the basis of the PMN-mediated effects by layering PMNs on bovine pulmonary artery endothelial monolayers. Challenge with OZ resulted in increased endothelial permeability to 125I-albumin. The monoclonal antibody IB4 (directed against CD18, the common beta-subunit of structurally related adhesion receptors on phagocytes, LFA-1, Mac-1, and P150,95) prevented the OZ-mediated increase in PMN adherence to endothelial cells and the increase in endothelial permeability to 125I-albumin. IB4 also inhibited the lung weight gain mediated by the OZ-stimulated PMNs in intact lungs. The protective effect of IB4 could be ascribed neither to inhibition of uptake of OZ by PMNs nor to inhibition of release of oxygen radicals, myeloperoxidase, and elastase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗