Release of proteases from cartilage cells as a result of activation by a macrophage factor--effects of some anti-inflammatory drugs.
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Animals↗
Biomedical subjects
K Phadke
Publications and source records attributed to K Phadke.
Defensive hostility and coronary heart disease: a preliminary investigation of male veterans.
OBJECTIVE: Research and theory link an interpersonal conflict model to cardiovascular disease. Specifically, persons scoring high on cynical hostility and social defensiveness are thought to manifest a defensive need for approval while harboring basic distrust and hostility toward those who could provide such approval. The objective of this study was to assess whether angiographically determined coronary artery disease (CAD) was associated with this combination of high cynical hostility and high social defensiveness. METHODS: Fifty-nine male patients of a Veterans Administration Medical Center (86% white, mean age = 59.9 years) participated in the study on the day before their angiographic procedure; these men filled out the Cook-Medley Hostility Scale and the Marlowe-Crowne Social Desirability Scale (social defensiveness). They subsequently were categorized as having defensive hostility (DH), high hostility (HH), high social defensiveness (SD), or low psychosocial risk (LRisk; low on both scales). RESULTS: The four groups did not differ significantly on risk factor status or health status. As predicted, a preplanned contrast showed that the DH group's mean number of arteries with at least 50% blockage (mean = 2.5) differed significantly from the combined means of the other groups. The HH and SD groups did not differ from the LRisk group. CONCLUSIONS: When combined with other reports, the approach-avoidance interpersonal conflict model holds the promise of providing additional information about the psychosocial factors contributing to CAD development among men with high cynical hostility.
Adult↗
Conditioned medium from a cell strain derived from a patient with mastocytosis induces the development of mature human mast cells in vitro from normal human bone marrow.
Mature human mast cells were obtained from human bone marrow in a coculture system using conditioned medium from a human mastocytosis cell strain. These cells expressed the high-affinity IgE receptor and were tryptase, chymase and carboxypeptidase positive.
Biomarkers↗
Rheumatic autoantibodies in the sera of patients with paraproteins.
OBJECTIVE: A high incidence of autoantibody activity has been previously described in the sera of patients with paraproteins. In this study we determined the incidence of autoantibodies of particular interest to rheumatologists (including antinuclear antibodies (ANA), anti-DNA, rheumatoid factor (RF), anticardiolipin antibodies (aCL) and the Sjögren's-related antibodies anti-SS.A/Ro and anti-SS.B/La) in the sera of patients with paraproteins, and the frequency with which the autoantibody activity isotype and the paraprotein isotype were identical. METHODS: ANA was determined by indirect immunofluorescence on HEp2 cells, anti-DNA by the Farr and Crithidia assays, aCL by ELISA, RF by nephelometry, antibodies to the extractable nuclear antigens (anti-ENA) by counter-immunoelectrophoresis (CIE), and anti-SS.B by immunoblot using a recombinant human SS.B antigen source. Incidences of these antibodies was compared in 3 groups of sera: 98 myeloma, 27 monoclonal gammopathy of uncertain significance (MGUS), and 24 age matched controls, using confidence interval analysis. RESULTS: There was no significant difference between the incidence of ANAs in paraprotein sera (8.8%) and control sera (16%). Neither was there a significant incidence of RF or aCL in the paraprotein sera. No anti-DNA antibodies were found and no anti-SS.B antibodies were found either with CIE or immunoblotting. Of the 11 ANAs detected in the paraprotein sera, isotype specific immunofluorescence suggested that 6 were monoclonal autoantibodies. CONCLUSIONS: These results indicate that the incidence of rheumatic autoantibodies is not raised in paraprotein sera compared to control sera. In particular, we could not confirm previous reports of a high incidence of anti-SS.B antibodies. However, of the ANAs detected half were monoclonal, unlike the polyclonality of the ANAs in the control group. That 4.8% of the paraproteins were monoclonal ANAs suggests that the process leading to paraproteinemia may activate usually silent autoreactive B cells as well as the normal B cell repertoire.
Arthritis, Rheumatoid↗