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Luminal acidification provides the strongest physiological stimulus for duodenal HC[O.sup.-.sub.3] secretion. Various neurohumoral mechanisms are believed to play a role in acid-stimulated HC[O.sup.-.sub.3] secretion. Previous studies in the rat and human duodenum have shown that guanylin and Escherichia coli heat-stable toxin, both ligands of the transmembrane guanylyl cyclase receptor [guanylate cyclase C (GC-C)], are potent stimulators for duodenal HC[O.sup.-.sub.3] secretion. We postulated that the GC-C receptor plays an important role in acid-stimulated HC[O.sup.-.sub.3] secretion. In vivo perfusion studies performed in wild-type (WT) and GC-C knockout (KO) mice indicated that acid-stimulated duodenal HC[O.sup.-.sub.3] secretion was significantly decreased in the GC-C KO animals compared with the WT counterparts. Pretreatment with PD-98059, an MEK inhibitor, resulted in attenuation of duodenal HC[O.sup.-.sub.3] secretion in response to acid stimulation in the WT mice with no further effect in the KO mice. In vitro cGMP generation studies demonstrated a significant and comparable increase in cGMP levels on acid exposure in the duodenum of both WT and KO mice. In addition, a rapid, time-dependent phosphorylation of ERK was observed with acid exposure in the duodenum of WT mice, whereas a marked attenuation in ERK phosphorylation was observed in the KO animals despite equivalent levels of ERK in both groups of animals. On the basis of these studies, we conclude that transmembrane GC-C is a key mediator of acid-stimulated duodenal HC[O.sup.-.sub.3] secretion. Furthermore, ERK phosphorylation may be an important intracellular mediator of duodenal HC[O.sup.-.sub.3] secretion. acid-stimulated bicarbonate secretion; extracellular signal-related kinase phosphorylation; intracellular signaling

Background: The colonic epithelium maintains a life long reciprocally beneficial interaction with the colonic microbiata. Disruption is associated with mucosal injury. Aims: We hypothesised that probiotics may limit epithelial damage [...]

Samples of corn grain with and without kelp meal and kelp extract were analyzed for IVDMD after a 72 h digestion in two trials. Trial 1 consisted of three treatments: 1) 100% corn grain, 2) 99% corn grain with 1% kelp meal, and 3) 98% corn grain with 2% kelp meal. Each treatment was inoculated with 1 mL of five different Erwinia concentration levels of 104, 105, 106, 107, and 108 cells. This trial was run in triplicate. One mL samples of fluid were withdrawn at 24, 28, and 72 h. Each fluid sample was then plated to calculate Erwinia survivability. Trial 2 consisted of three treatments: 1) 100% corn grain, 2) 99% corn grain with 1% kelp extract, and 3) 98% corn grain with 2% kelp extract. Each treatment was conducted in multiples of 7. After digestion, samples were dried for 72 hours at 50 [degrees] C. Samples were weighed after reaching thermal equilibrium and analyzed for IVDMD. Data were analyzed using the GLM procedures of SAS. In Trial 1, the average IVDMD of all samples that contained no kelp meal was 90.39%. The IVDMD was reduced when kelp meal was added at 1% to 78.8% (P Key Words: Beef cattle, Kelp, In vitro digestibility

Background: The colonic epithelium maintains a life long reciprocally beneficial interaction with the colonic microbiota. Disruption is associated with mucosal injury. Aims: We hypothesised that probiotics may limit epithelial damage induced by enteroinvasive pathogens, and promote restitution. Methods: Human intestinal epithelial cell lines (HT29/cl. 19A and Caco-2) were exposed to enteroinvasive Escherichia coli (EIEC 029:NM), and/or probiotics (Streptococcus thermophilus (ST), ATCC19258, and Lactobacillus acidophilus (LA), ATCC4356). Infected cells and controls were assessed for transepithelial resistance, chloride secretory responses, alterations in cytoskeletal and tight junctional proteins, and responses to epidermal growth factor (EGF) stimulation. Results: Exposure of cell monolayers to live ST/LA, but not to heat inactivated ST/LA, significantly limited adhesion, invasion, and physiological dysfunction induced by EIEC. Antibiotic killed ST/LA reduced adhesion somewhat but were less effective in limiting the consequences of EIEC invasion of cell monolayers. Furthermore, live ST/LA alone increased transepithelial resistance, contrasting markedly with the fall in resistance evoked by EIEC infection, which could also be blocked by live ST/LA. The effect of ST/LA on resistance was accompanied by maintenance (actin, ZO-1) or enhancement (actinin, occludin) of cytoskeletal and tight junctional protein phosphorylation. ST/LA had no effect on chloride secretion by themselves but reversed the increase in basal secretion evoked by EIEC. EIEC also reduced the ability of EGF to activate its receptor, which was reversed by ST/LA. Conclusions: Live ST/LA interact with intestinal epithelial cells to protect them from the deleterious effect of EIEC via mechanisms that include, but are not limited to, interference with pathogen adhesion and invasion. Probiotics likely also enhance the barrier function of naïve epithelial cells not exposed to any pathogen. [ABSTRACT FROM AUTHOR]

Describes an algorithm for the solution of two simultaneous quadratic equations in two variables. Requirement of the algorithm of a solution of a quartic equation in one variable; Illustration of the standard explicit formula for solving the problem; Equations used in the intersection of two conics.