Pediatric barium enema examination: Optimizing patient selection with univariate and multivariate analyses

We prospectively evaluated a total of nineteen symptoms, signs, and laboratory findings in 471 of 557 consecutive pediatric patients (from newborn to age 17) referred for barium enema examinations, to determine predictors of an abnormal study. A univariate analysis was performed, and a logistic regression model was developed. The most frequent indicators for the barium enema examinations were abdominal pain (48%), constipation (27%) and tenderness (25%). Twenty-two percent of the examination were abnormal, and the most common diagnoses were intussusception (n=22), appendicitis (n=17), infectious colitis (n=15), and Hirschsprung disease (n=14). The indicators that were most helpful to predict a barium enema abnormality were abdominal mass, leukocytosis, guaiac-positive stools, diarrhea, anemia, tenderness, and age less than 1 year. If barium enema examinations were performed only when at least one of the predictive indicators was present, 29% of examinations would be eliminated, and 4.8% of patients with detectable disease would be missed. The data indicate that identification of certain clinical variables can provide an effective initial strategy for selecting patients to undergo barium enema examinations.     

Tumor Necrosis Factor-α Blocks Differentiation and Enhances Suppressive Activity of Immature Myeloid Cells during Chronic Inflammation

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Highlights? TNF-α promotes immunosuppression during chronic inflammation via MDSCs ? TNF-α blocks MDSC maturation by enhancing S100A8/9 and RAGE expression ? TNF-α augments MDSC suppressive activity impairing T and NK cell function ? Etanercept enhances MDSC maturation and reduces their suppressive activity     

A transfected m5 muscarinic acetylcholine receptor stimulates phospholipase A2 by inducing both calcium influx and activation of protein kinase C

Receptor-mediated arachidonic acid release and its relationship to phospholipase A2 and phospholipase C activation were investigated in Chinese hamster ovary cells transfected with and expressing the m5 muscarinic receptor. Carbachol, a muscarinic receptor agonist, stimulated the release of arachidonic acid and inositol phosphates with similar potencies. In addition, carbachol and the phorbol ester, phorbol-12-myristate, 13-acetate (PMA), stimulated protein kinase C (PKC) activity. PMA potentiated the carbachol-stimulated release of arachidonic acid, but had no effect on release of inositol phosphates. Long-term preincubation with PMA or carbachol inhibited PKC activity and prevented carbachol-stimulated release of arachidonic acid, but not inositol phosphates, suggesting that release of arachidonic acid, but not release of inositol phosphates, required activation of PKC. Carbachol stimulated the release of [3H]lysophosphatidylcholine from [3H]choline prelabeled cells, suggesting that phospholipase A2 was involved in the release of arachidonic acid. The role of calcium in carbachol-stimulated release of arachidonic acid was also investigated. Carbachol stimulated a transient followed by a sustained increase in intracellular calcium. In the absence of extracellular calcium, the transient rise in intracellular calcium was maintained but the sustained increase in intracellular calcium and the release of arachidonic acid were abolished. Carbachol stimulated a sustained influx of 45Ca++. We conclude that the combined effect of PKC activation and sustained elevation of intracellular calcium, from an extracellular source, is essential for m5 muscarinic receptor activation of phospholipase A2.