T Durbin

Long Beach Memorial Medical Center, Long Beach, California, United States

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Publications (3)20.21 Total impact

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    ABSTRACT: Expression of epidermal growth factor receptor (EGFR) was studied immunohistochemically in rat gastric mucosa during healing of acetic acid-induced ulcers. In normal control gastric oxyntic mucosa, EGFR was expressed in proliferative zone cells and in some parietal cells. In mucosa of the ulcer margin, at 3, 7, and 16 days after ulcer induction, there was a 75-fold increase (over controls) in the number of cells expressing EGFR. Seventy percent of ulcers healed by the 16th day, and all were healed by the 25th day. The mucosal scar that replaced the ulcer was composed of dilated glands lined with poorly or aberrantly differentiated cells showing persistence of increased EGFR expression. An increased EGFR expression indicates an important role of EGF in ulcer healing and scar formation.
    Gastroenterology 03/1992; 102(2):695-8. · 16.72 Impact Factor
  • T Fukuda · T Arakawa · T Mach · T Durbin · A Tarnawski
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    ABSTRACT: We investigated the effects of calcium channel blockers on generation of prostaglandin (PG) E2 and 6-keto PGF1 alpha by gastric mucosal surface epithelium. Surface epithelial cells (SEC) isolated from rat gastric mucosa were incubated with either verapamil (1 or 10 micrograms/ml), diltiazem (2.5 or 25 micrograms/ml) or nifedipine (2.5 or 25 micrograms/ml) for 30 min at 37 degrees C in calcium containing or calcium-free medium. Verapamil (both doses) significantly increased PGE2 and 6-keto PGF1 alpha generation by the surface epithelial cells but only in calcium containing medium. Diltiazem did not affect PG generation in calcium containing nor calcium-free medium. Nifedipine 25 micrograms/ml decreased PGE2 but increased 6-keto PGF1 alpha generation. The inhibitory effect of nifedipine on PGE2 generation was abolished in calcium-free medium, while the calmodulin antagonist did not affect verapamil-induced increase in PG generation.
    Prostaglandins 01/1992; 42(6):587-97. DOI:10.1016/0090-6980(91)90020-G
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    ABSTRACT: Epidermal growth factor (EGF) is a mitogenic polypeptide that inhibits gastric acid secretion, protects the gastric mucosa against acute injury, and accelerates ulcer healing. In the present study we demonstrated immunohistochemically, using two different techniques, localization of EGF receptors in normal rat gastric oxyntic mucosa: in proliferative zone cells and in some parietal cells. It is likely that these cells represent the major targets for the EGF [and transforming growth factor alpha (TGF-alpha) which shares a common receptor with EGF] actions, stimulating cell proliferation and inhibiting acid secretion.
    Journal of Clinical Gastroenterology 02/1991; 13 Suppl 1:S109-13. DOI:10.1097/00004836-199112001-00018 · 3.50 Impact Factor

Publication Stats

139 Citations
20.21 Total Impact Points


  • 1992
    • Long Beach Memorial Medical Center
      Long Beach, California, United States
    • United States Department of Veterans Affairs
      Бедфорд, Massachusetts, United States