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Biomedical subjects

J O Shaw

Publications and source records attributed to J O Shaw.

26 records · Page 2Linked to original sources
PubMed1979

Macrophage-mediated tumor cell killing: lack of dependence on the cyclooxygenase pathway of prostaglandin synthesis.

M phi obtained directly from disaggregated murine Moloney sarcomas produced PGE2 and a hydroxy fatty acid derivative as the major products of arachidonic acid metabolism. M phi-immunoreactive PGE synthetic rates decreased substantially and cytotoxic activity was lost when freshly explanted tumor M phi were held in culture 24 hr. Such cultured M phi remained in a partially activated "primed" state, however, wherein the addition of minute (ng) amounts of bacterial lipopolysaccharide (LPS) returned cytolytic activity and PGE synthesis to original levels. Indomethacin-induced blockade of the M phi cyclooxygenase pathway inhibited PG synthesis by LPS-stimulated, primed M phi without affecting the return of cytolytic activity. We conclude, therefore, that the production of PG had no direct role in the mediation of tumor cell killing by activated M phi isolated from these neoplasms.

Animals↗
PubMed1979

Complement fragments, alveolar macrophages, and alveolitis.

Mechanisms of neutrophil infiltration into the rabbit alveolus have been investigated. Complement activation in the circulation induced pulmonary vascular margination but not a significant level of alveolar infiltration. Instillation of C5 fragments into the airways, however, attracted neutrophils into the alveolar airspaces. The anaphylatoxin-inactive fragment of C5, C5a des Arg, was found to be much more active in this regard than C5a. Furthermore, these fragments were shown to induce the production of a neutrophil-directed chemoctactic factor from pulmonary macrophages, raising the question of whether the C5a des Arg was acting directly to attract neutrophils or indirectly via the macrophage. To substantiate a possible role for C5 and C5 fragments in alveolitis, active C5 was demonstrated in lavage fluids, and macrophage-derived C5 cleaving enzymes have been described. Finally, a route of neutrophil infiltration via migration through the alveolar capillary wall into the interstitium is proposed, and subsequent penetration of the alveolar epithelium out into the airspace. (Am J Pathol 97:93--110, 1979).

Alveolitis, Extrinsic Allergic↗
PubMed1978

The influence of nitrous oxide anaesthetic on middle-ear fluid.

Nitrous oxide anaesthesia invades the middle-ear cavity, resulting in a positive pressure within this cavity. It has been suggested that the pressure may be sufficient to force open the Eustachian tube and evacuate fluid from the middle ear. This study examined the possible influence of nitrous oxide on middle-ear fluid. Pre- and intra-operative tympanograms were obtained on 39 children scheduled for myringotomy surgery. Fluid was found in 83.1% of the operated ears while the absence of fluid was noted in 16.9%. It is possible that the nitrous oxide anaesthetic did cause an evacuation of fluid from this latter group of ears prior to actual surgery.

Acoustic Impedance Tests↗
PubMed1978

Phospholipase A2 contamination of cobra venom factor preparations. Biologic role in complement-dependent in vivo reactions and inactivation with p-bromophenacyl bromide.

Cobra venom factor (CoF), the anticomplementary protein in Naja naja cobra venom, is usually purified by sequential ion exchange and gel filtration chromatography. CoF prepared in this manner contains small but significant quantities of phospholipase A2 activity. This acyl hydrolase activity can be simply and efficiently removed on a large scale by treatment of CoF with p-bromophenacyl bromide (BPB), an irreversible modifier of the histidine residue in the active site of phospholipase A2. BPB treatment does not alter the anticomplementary activity of CoF. In vivo experiments utilizing intratracheal injections of control and BPB-treated CoF, as well as pure phospholipase A2, revealed that contaminating phospholipase A2, and not the anticomplementary protein, was responsible for the observed acute neutrophil-associated lung injury. However, phospholipase A2 had no effect on the hypotensive and thrombocytopenic effects of CoF infected intravenously into rabbits. Depletion of circulating C3-C9 by intraperitoneal injections of CoF was not altered by removal of phospholipase A2 activity with BPB.

Acetophenones↗
PubMed1977

Intravascular aggregation and pulmonary sequestration of platelets during IgE-induced systemic anaphylaxis in the rabbit: abrogation of lethal anaphylactic shock by platelet depletion.

Significant alterations in the circulatory properties of platelets have been documented during IgE-induced systemic anaphylactic shock in the rabbit. Within 30 to 60 sec after i.v. antigen challenge, platelet aggregation occurs in both the venous and arterial circulations. The platelet aggregates then sequester in small blood vessels of various organs, particularly in the lung. The organ sequestration results in the development of a profound thrombocytopenia within 3 to 5 min after antigen challenge. Fifteen min later deaggregation of platelets occurs and the platelets return to the peripheral circulation within normal, prechallenge levels by 60 min. Additional experiments demonstrated that platelet depletion before antigen challenge abrogates the lethal effects and significantly reduces the pathophysiologic manifestations of IgE-induced systemic anaphylaxis. We conclude that the IgE-induced platelet alterations, probably induced by the intravascular release of basophil and perhaps mast cell-derived platelet-activating factor (PAF), play a major role in the pathogenesis of systemic anaphylaxis in the rabbit.

Anaphylaxis↗
PubMed1975

The current status of prostaglandins and the lungs.

The prostaglandins are a group of pharmacologically potent lipid compounds whose role in pulmonary pathophysiology remains to be defined. There is not question that these compounds can induce constriction (PGF) or relaxation (PGE) of the smooth muscle in bronchi and pulmonary vessels. There is no question that the lungs are a major site of both the synthesis and degradation. These facts make speculation about the role of the prostaglandins in pulmonary disorders a tempting exercise. However, the current paucity of clinical data prevents any valid assessment of such speculation at this time and emphasizes the need for continued investigation of the role of prostaglandins in patients with lung disease.

Animals↗