Publications by authors named "A C Bylund-Fellenius"

Background: Animal models of inflammatory bowel disease are artificial and more or less representative of human disease. However, the dextran sulphate sodium (DSS) induced intestinal inflammation model has recently been shown to fulfil some pathological criteria for an adequate experimental model.

Aim: To determine whether this form of experimental intestinal inflammation responds to established therapy used for human inflammatory bowel disease.

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Administration of dextran sulfate to mice, given in the drinking water results in acute or subacute colonic inflammation, depending on the administration protocol. This colonic inflammation exhibits ulceration, healing and repair, and a therapeutic response that makes it valuable for the study of mechanisms that could act in the pathogenesis of human ulcerative colitis, a disease thought to have an immunologically dependent pathogenesis. To investigate if immunological mechanisms were involved in the induction of colonic inflammation in this model, mice with different degrees of immunodeficiency were used.

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Intravital fluorescence microscopy and morphometry were used to study the microcirculation in the rat gastric mucosa during and after hemorrhagic shock. Under control conditions the circulation appeared homogeneous and unaffected by superfusion with 0.1 N HCl.

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Optimal conditions for simultaneous analysis of the purine nucleotides adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), inosine monophosphate (IMP), inosine, adenosine, hypoxanthine, xanthine and uric acid in muscle samples by high-performance liquid chromatography (HPLC) were evaluated. A neutralized perchloric acid extract of freeze-dried human or rat skeletal muscle tissue was injected on to a reversed-phase silica column and eluted by a gradient composed of ammonium dihydrogen phosphate buffer and methanol. Good resolution for all the nucleotides was achieved within a retention time of about 20 min.

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An in vivo rat hindlimb tourniquet ischemia model was used to study the purine nucleotide metabolism in response to 2, 4, and 6 h of ischemia and to the same ischemia periods followed by 1 h of reperfusion. All purine intermediates from ATP to uric acid were determined in skeletal muscle with a high-performance liquid chromatography (HPLC) system. The major metabolic event during ischemia is to temporarily save the nucleotide pool as inosine-5'-monophosphate (IMP.

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