Owen Tully

Lankenau Institute for Medical Research, Wynnewood, Oklahoma, United States

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Publications (7)26.82 Total impact

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    ABSTRACT: To determine if the observed paracellular sucrose leak in Barrett's esophagus patients is due to their proton pump inhibitor (PPI) use. The in vivo sucrose permeability test was administered to healthy controls, to Barrett's patients and to non-Barrett's patients on continuous PPI therapy. Degree of leak was tested for correlation with presence of Barrett's, use of PPIs, and length of Barrett's segment and duration of PPI use. Barrett's patients manifested a near 3-fold greater, upper gastrointestinal sucrose leak than healthy controls. A decrease of sucrose leak was observed in Barrett's patients who ceased PPI use for 7 d. Although initial introduction of PPI use (in a PPI-naïve population) results in dramatic increase in sucrose leak, long-term, continuous PPI use manifested a slow spontaneous decline in leak. The sucrose leak observed in Barrett's patients showed no correlation to the amount of Barrett's tissue present in the esophagus. Although future research is needed to determine the degree of paracellular leak in actual Barrett's mucosa, the relatively high degree of leak observed with in vivo sucrose permeability measurement of Barrett's patients reflects their PPI use and not their Barrett's tissue per se.
    World Journal of Gastroenterology 06/2012; 18(22):2793-7. · 2.43 Impact Factor
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    ABSTRACT: Colorectal cancer (CRC) is one of the most common cancers in the western world. Early screening and detection could be highly preventative and therefore reduce mortality. Tight junctions (TJ) are well known for their function in controlling paracellular traffic of ions and molecules. It has become increasingly evident that TJs play a crucial role in maintaining cell-cell integrity, and the loss of cell junctional sealing could involve itself in the processes of carcinoma and cancer metastasis. If correlations between altered TJ proteins and CRC presence or invasiveness could be established, they may serve as important markers and guidelines for prophylactic and prognostic purposes, along with other screening methods. This review will present recent data from clinical and animal studies showing how altered TJ protein expression is a feature of certain CRCs. The up-regulation of claudin-1 in many CRCs is especially noteworthy. The focus of this article is simply on the association - however imperfect - between CRC and the major TJ transmembrane barrier proteins, namely claudins and occludin. Any causal relationship between TJ protein change and neoplasia remains conclusively unproven at present.
    The Scientific World Journal 01/2011; 11:826-41. · 1.22 Impact Factor
  • Gastrointestinal Endoscopy 04/2009; 69(5). · 4.90 Impact Factor
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    ABSTRACT: Proton pump inhibitors (PPIs) are one of the most widely used drug classes in the US and are now frontline medications for gastro-oesophageal reflux disease (GERD) and dyspepsia. In a previous work, we observed that a transmucosal, upper gastrointestinal (GI) leak exists in Barrett's oesophagus (BO) patients. PPI medications are commonly used by Barrett's patients. To examine if the PPI, esomeprazole, affects the barrier function of the upper GI tract. The sucrose permeability test (SPT) was used to assess the possible effect of the PPI, esomeprazole, on upper GI leak in 37 first-time-presenting GERD patients and 25 healthy controls. Esomeprazole induced a significant transmucosal leak in the upper GI tract of patients taking the drug for the first time. The leak occurred quickly, within days of first taking the drug. The leak was also reversed within days of stopping the medication. This is the first patient-based study showing that a PPI compromises upper GI barrier function. There are potential implications for transmucosal leak of other medications that a patient on a PPI may be taking, as well as possible leak of endogenous peptides/proteins. The clinical consequences of this phenomenon are currently unknown, but are potentially important.
    Alimentary Pharmacology & Therapeutics 09/2008; 28(11-12):1317-25. · 4.55 Impact Factor
  • Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 09/2008; 7(3):A26. · 5.64 Impact Factor
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    ABSTRACT: To evaluate the presence of Na+-dependent, active, sugar transport in Barrett's epithelia as an intestinal biomarker, based on the well-documented, morphological intestinal phenotype of Barrett's esophagus (BE). We examined uptake of the nonmeta-bolizable glucose analogue, alpha-methyl-D-glucoside (AMG), a substrate for the entire sodium glucose cotransporter (SGLT) family of transport proteins. During upper endoscopy, patients with BE or with uncomplicated gastroesophageal reflux disease (GERD) allowed for duodenal, gastric fundic, and esophageal mucosal biopsies to be taken. Biopsies were incubated in bicarbonate-buffered saline (KRB) containing 0.1 mmol/L 14C-AMG for 60 min at 20 centigrade. Characterized by abundant SGLT, duodenum served as a positive control while gastric fundus and normal esophagus, known to lack SGLT, served as negative controls. Duodenal biopsies accumulated 249.84+/-35.49 (SEM) picomoles AMG/microg DNA (n=12), gastric fundus biopsies 36.20+/-6.62 (n=12), normal esophagus 12.10+/-0.59 (n=3) and Barrett's metaplasia 29.79+/-5.77 (n=8). There was a statistical difference (P<0.01) between biopsies from duodenum and each other biopsy site but there was no statistically significant difference between normal esophagus and BE biopsies. 0.5 mmol/L phlorizin (PZ) inhibited AMG uptake into duodenal mucosa by over 89%, but had no significant effect on AMG uptake into gastric fundus, normal esophagus, or Barrett's tissue. In the absence of Na+ (all Na+ salts replaced by Li+ salts), AMG uptake in duodenum was decreased by over 90%, while uptake into gastric, esophageal or Barrett's tissue was statistically unaffected. Despite the intestinal enterocyte phenotype of BE, Na+-dependent, sugar transport activity is not present in these cells.
    World Journal of Gastroenterology 04/2008; 14(9):1365-9. · 2.43 Impact Factor
  • Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 05/2007; 5(4):A26. · 5.64 Impact Factor