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We previously described a murine model of malnutrition that mimicked features of moderate human malnutrition, and led to increased dissemination of Leishmania donovani. In this study, we investigated the effect of malnutrition on macrophage production of cytokines, prostaglandins (PGs), and leukotrienes (LTs). Using either LPS or calcium ionophore A23187 as a stimulus, macrophages from the malnourished mice produced a 3-fold higher PG/LT ((PGE(2)+6-keto-PGF(1alpha))/(LTB(4)+cysteinyl leukotrienes)) ratio than macrophages from well-nourished mice.

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The potential relationship of an intact membrane organization to the synthesis of chondroitin was examined before and after modification of a chick-embryo cartilage microsomal system with the non-ionic detergent Triton X-100. Incubations with labelled UDP-GlcA and UDP-GalNAc indicated that Triton X-100 had little effect on the amount of chondroitin synthesized to form one species of large proteochondroitin (Type I). However, Triton X-100 had a marked stimulatory effect on the formation of another smaller species of proteochondroitin (Type II).

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Thermal injury causes directly a liberation of inositolphosphates, diacylglycerols, free arachidonic acid, and lyso PAF from eukaryotic cells. From lyso PAF derivates PAF, from free arachidonic acid are derivating PG, LT, and TX. These "soluble mediators" are stimulating inflammatory cell populations in a feedback mechanism: the stimulus activates the inflammatory cells to produce the same soluble mediators (Fig.

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