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Functional abdominal pain (FAP) is one of the most common functional gastrointestinal disorders (FGIDs) of childhood. Only a minority of patients with FAP seek medical attention, often presenting to the primary care physician while symptoms are still evolving. The bio-psychosocial model of treatment not only aims to alleviate the illness symptoms but also identifies and remedies the psychological comorbidities and social factors that contribute to illness behavior. Many patients with a mild illness can be managed in the primary care setting. However those with chronic, severe, frequently relapsing, and disabling illness usually are referred to a pediatric gastroenterologist. One of the reason for referral is to exclude organic disorders such as peptic ulcer disease, celiac disease or inflammatory bowel disease which can present with chronic abdominal pain. Recent data suggest that psychological therapy is very effective in alleviating symptoms, a subset of patients may require dietary modification and medications as an adjunct to psychological treatment.

Despite lack of standardized diagnostic criteria and variable outcomes of surgical intervention reported in pediatric literature, cholecystectomies are commonly performed for children with BD in the United States. Consensus guidelines for the diagnosis and management of this controversial disorder in children are needed.

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Experimental myocardial infarction is typically determined using TTC. TTC, reduced to a red product in intact cells by endogenous enzymes/cofactors, remains colorless in damaged cells from which the enzymes/cofactors have been removed during reperfusion. Its use is limited to studies with prolonged reperfusion and sections cannot be used for other pathological events. Two recent studies showed that propidium iodide (PI), which enters damaged cells and intercalates with DNA to produce a red fluorescent complex, can be injected in vivo following ischemia/reperfusion to assess infarct size. We build on this in a murine model, using PI to study early infarct development and to evaluate the concurrent inflammatory response as indicated by complement C3 deposition. Occlusion of the coronary artery was followed by increasing periods of reperfusion and injection of PI to define infarction. Blue fluorescent microspheres were injected to define the area at risk (AAR). Heart slices were immediately imaged for infarction and AAR, and cryosections obtained from the slices imaged for C3 using FITC-labeled antibody. PI fluorescence revealed a significant infarction at 1 hour of reperfusion which was maintained through 24 hours. C3 deposition lagged infarction development, becoming significant at 3 hours of reperfusion. In summary, in vivo injection of PI allows study of the early stages of infarction and permits analysis, in the same tissue, of concurrently occurring inflammatory events.

No abstract