Hamburger-associated Escherichia coli O157:H7 infection in Las Vegas: a hidden epidemic.

Objectives: This study sought to determine whether a multistate fast food hamburger-associated outbreak of Escherichia coli O157:H7 infection involved Las Vegas residents as well and, if so, why public health officials had not detected it.

Methods: A matched case-control study was conducted among persons with bloody diarrhea and their healthy meal companions. Hamburger production, distribution, and cooking methods were reviewed.

A novel colon-specific steroid prodrug enhances sodium chloride absorption in rat colitis.

A recently synthesized novel colon-specific dexamethasone prodrug, dexamethasone-beta-D-glucuronide, delivers efficacious amounts of dexamethasone to the colon with limited adrenal suppressive effects. During experimentally induced colitis in rats, the dexamethasone prodrug is significantly more potent than free dexamethasone in improving colonic fluid and electrolyte absorptive injury. The present studies examined whether the improvement in colonic absorption seen with the prodrug occurred as a consequence of alterations in sodium and chloride epithelial transport.

Colonic delivery of dexamethasone from a prodrug accelerates healing of colitis in rats without adrenal suppression.

Background/aims: Dexamethasone-beta-D-glucuronide, a colon-specific prodrug of dexamethasone, may be useful in the treatment of ulcerative colitis and Crohn's colitis. The aim of this study was to evaluate colonic delivery and efficacy of this prodrug in the rat.

Methods: Distribution of dexamethasone in luminal contents and tissues of the gastrointestinal tract and in plasma was measured after oral administration of dexamethasone-beta-D-glucuronide or free dexamethasone.

Acetic acid-induced colitis results in bystander ileal injury.

The extent of the small intestinal injury following experimental acetic acid induction of colitis in rats was examined. Following intraluminal colonic administration of radiolabelled acetic acid, high levels of radioactivity were identified in the colon and in the liver, while low background levels were found in jejunum, ileum, caecum, and heart. The increased level of radioactivity in the liver relative to that of the heart suggests that a significant portion of the colonic intraluminal acetic acid was absorbed directly into the portal circulation.

Indomethacin worsens and a leukotriene biosynthesis inhibitor accelerates mucosal healing in rat colitis.

The implication of leukotrienes as mediators of inflammation and recent evidence that prostaglandin analogues provide a beneficial effect during experimental colitis led to the speculation that (i) leukotrienes may be injurious and (ii) prostaglandins may be protective to colonic mucosa. Using a 2% acetic acid induced rat colitis model, we administered specific cyclooxygenase (indomethacin) and leukotriene biosynthesis inhibitors (MK-886) to examine the effect of endogenous prostaglandins and leukotrienes on colonic macroscopic injury, mucosal inflammation as measured by myeloperoxidase activity, net in vivo intestinal fluid absorption, and colonic PGE2 and LTB4 levels as measured by in vivo rectal dialysis. Indomethacin treatment prior to induction of colitis reduced endogenous mucosal PGE2 levels and exacerbated macroscopic ulceration and net fluid absorption.