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Biomedical subjects

C A Stewart

Publications and source records attributed to C A Stewart.

97 records · Page 6Linked to original sources

Systemic form of Weber-Christian disease.

A case of systemic Weber-Christian disease, involving retroperitoneal adipose tissue with secondary damage to the associated organs and blood vessels is reported. The involved organs showed varying degrees of necrosis, lipogranulomata and fibrosis.

Adipose Tissue↗

Enhancing the recognition and production of facial expressions of emotion by children with mental retardation.

The ability to recognize and respond appropriately to facial expressions of emotion is essential for interpersonal interaction. Individuals with mental retardation have problems not only in recognizing but also in accurately producing facial expressions of emotion. In Experiment 1, directed rehearsal was used to teach six boys with mild and moderate mental retardation to increase their ability to recognize facial expressions of emotion. In addition, their ability to produce the six basic facial expressions of emotion was periodically assessed throughout the study. The results showed that the boys' accuracy in recognizing facial expressions of emotion increased rapidly with instruction and that their increased accuracy was maintained at 8- and 12-week assessments following the termination of instruction. However, their increased levels of recognition did not generalize to the production of these emotions. In Experiment 2, four boys who had participated in the first study were provided with directed rehearsal training in the production of the six basic facial expressions of emotion. Their ability to produce facial expressions of emotion increased with instruction and was maintained following the termination of instruction. In addition, independent raters judged that the boys' production of these emotions matched the emotions that they were required to produce, suggesting a socially valid behavior change. These studies showed that the ability of children with mental retardation to recognize and produce facial expressions of emotion can be enhanced through instruction.

Adolescent↗

Tumor-derived recognition factor (TDRF) induces production of TNF-alpha by murine macrophages, but requires synergy with IFN-gamma alone or in combination with IL-2 to induce nitric oxide synthase.

A constitutively produced soluble activity, designated tumor-derived recognition factor (TDRF), from L1210, P815 and EL4 tumor targets, was previously shown to synergize with interferon-gamma (IFN-gamma) and subactivating concentrations of interleukin-2 (IL-2) to induce murine macrophage production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) for cytotoxicity of the target of origin. Another study had suggested that TDRF upregulated both TNF-alpha receptor (TNF-alpha R) and IFN-gamma receptor (IFN-gamma R) mRNA synthesis, as well as increased TNF-alpha and IFN-gamma binding to their receptors. In the present study, we have further characterized the concentration-dependent macrophage activating potential of TDRF alone and in synergy with IFN-gamma or IFN-gamma and subactivating concentrations of IL-2. Higher concentrations of TDRF acted independently on inflammatory C3H FeJ mouse macrophage to induce expression of TNF-alpha mRNA and release of TNF-alpha, but failed to induce nitric oxide synthase (NOS) mRNA expression and NO generation. At lower concentrations, TDRF synergized with either IFN-gamma alone or in combination with IL-2 to stimulate a dose-related increase in the expression of TNF-alpha mRNA and secretion of TNF-alpha, as well as increased induction of NOS mRNA and cytotoxic NO generation by macrophage. MCA tumor targets which did not produce TDRF activity were killed by macrophage that had been activated by exogenously added L1210-derived TDRF in synergy with IFN-gamma or in combination with subactivating concentrations of IL-2, but not by TDRF alone. Taken together, our results indicate that TDRF acted independently in a dose-dependent fashion to induce macrophage synthesis and release of TNF-alpha, but in the absence of IFN-gamma or in combination with IL-2 failed to induce the NOS enzyme which was necessary for cytotoxic NO generation. Thus TDRF appears to be a sufficient second signal for IFN-gamma-primed macrophage or alternatively a sufficient third signal for IFN-gamma and IL-2 treated macrophage to culminate the activation process for NOS mRNA synthesis and NO-mediated tumor cytotoxicity.

Animals↗