Comparison of two different stool antigen tests for the primary diagnosis of Helicobacter pylori infection in turkish patients with dyspepsia

AIM: To assess the reliability of two different enzyme immunoassays in detecting the Helicobacter pylori status in stool specimens of Turkish patients with dyspepsia. MATERIALS AND METHODS: One hundred and fifty-one patients [74 with nonulcer dyspepsia (NUD), 64 with duodenal ulcer (DU) and 13 with gastric cancer] who were admitted to the endoscopy unit of Istanbul University, Cerrahpasa Medical Faculty for upper gastrointestinal endoscopy because of dyspepsia were enrolled in the study. Helicobacter pylori infection was confirmed in all patients by histology, rapid urease test and culture. A patient was classified as being H. pylori-positive if the culture alone or both the histology and the rapid urease test were positive and as negative only if all of these tests remained negative. Stool samples were obtained from patients to assess the reliability of a monoclonal (FemtoLab H. pylori) and a polyclonal (Premier Platinum HpSA) stool antigen test and to compare the diagnostic accuracies of these two tests. A chi2 test was used for statistical comparisons. RESULTS: Using cut-off values of 0.19 for FemtoLab H. pylori and 0.16 for Premier Platinum HpSA, the sensitivity, specificity, positive predictive value, negative predictive value and diagnostic accuracy were 93%, 90%, 98%, 68% and 93% for the monoclonal test and 84%, 67%, 94%, 40% and 81% for the polyclonal test, respectively. The sensitivity, specificity, negative predictive value and diagnostic accuracy of the monoclonal test were significantly greater than those of the polyclonal test (chi2 = 3.98; p < .05 for sensitivity and chi2 = 15.67; p = .000 for specificity, chi2 = 15.78; p = .000 for negative predictive value and chi2 = 6.37; p = .012 for diagnostic accuracy). The bacterial load did not affect the sensitivity of either test. CONCLUSIONS: The monoclonal FemtoLab H pylori test, using a cut-off 0.19, is a very sensitive, specific and easy to perform diagnostic tool for the primary diagnosis of H. pylori infection in Turkish patients with dyspepsia.     

Nitric oxide-dependent generation of reactive species in sickle cell disease. Actin tyrosine induces defective cytoskeletal polymerization

The intermittent vascular occlusion occurring in sickle cell disease (SCD) leads to ischemia-reperfusion injury and activation of inflammatory processes including enhanced production of reactive oxygen species and increased expression of inducible nitric-oxide synthase (NOS2). Appreciating that impaired nitric oxide-dependent vascular function and the concomitant formation of oxidizing and nitrating species occur in concert with increased rates of tissue reactive oxygen species production, liver and kidney NOS2 expression, tissue 3-nitrotyrosine (NO(2)Tyr) formation and apoptosis were evaluated in human SCD tissues and a murine model of SCD. Liver and kidney NOS2 expression and NO(2)Tyr immunoreactivity were significantly increased in SCD mice and humans, but not in nondiseased tissues. TdT-mediated nick end-label (TUNEL) staining showed apoptotic cells in regions expressing elevated levels of NOS2 and NO(2)Tyr in all SCD tissues. Gas chromatography mass spectrometry analysis revealed increased plasma protein NO(2)Tyr content and increased levels of hepatic and renal protein NO(2)Tyr derivatives in SCD (21.4 +/- 2.6 and 37.5 +/- 7.8 ng/mg) versus wild type mice (8.2 +/- 2.2 and 10 +/- 1.2 ng/mg), respectively. Western blot analysis and immunoprecipitation of SCD mouse liver and kidney proteins revealed one principal NO(2)Tyr-containing protein of 42 kDa, compared with controls. Enzymatic in-gel digestion and MALDI-TOF mass spectrometry identified this nitrated protein as actin. Electrospray ionization and fragment analysis by tandem mass spectrometry revealed that 3 of 15 actin tyrosine residues are nitrated (Tyr(91), Tyr(198), and Tyr(240)) at positions that significantly modify actin assembly. Confocal microscopy of SCD human and mouse tissues revealed that nitration led to morphologically distinct disorganization of filamentous actin. In aggregate, we have observed that the hemoglobin point mutation of sickle cell disease that mediates hemoglobin polymerization defects is translated, via inflammatory oxidant reactions, into defective cytoskeletal polymerization.     

Healing-promoting effect of bombesin treatment on chronic gastric ulcer in rats

To evaluate whether bombesin treatment has a facilitatory effect on the healing of chronic gastric ulcer, following the induction of ulcer by serosal application of acetic acid, rats were given bombesin (30 microg/kg/day; subcutaneously) or vehicle three times a day for 7, 14 or 21 days until they were decapitated. Neither food intake nor gastric emptying rate in either vehicle-treated or bombesin-treated groups was not statistically different from control rats. Similarly, ulcer indices and gastric myeloperoxidase (MPO) activities at the first and second weeks of injury were not different among the groups. However, in the 3-week ulcer group, bombesin treatment reduced tissue MPO level significantly back to control levels. Moreover, the analysis of the surface epithelium by scanning electron and light microscopy demonstrated a significant reduction in the severity of ulcers by bombesin treatment. Pretreatment with CCK antagonists (L-364,718 or L365,260; 25 micromol/kg/day) before bombesin treatment showed that neither of the CCK antagonists had a significant effect on the bombesin-mediated healing process, suggesting that CCK receptors are not involved in the action of bombesin. In accordance with the previous studies that show its acute gastroprotective effects, bombesin is also effective in promoting the healing process of chronic gastric ulcer in rats.