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Currently, there are no high-resolution impedance manometry (HRIM)-based diagnostic criteria for non-obstructive dysphagia (NOD). New impedance parameters, such as the esophageal impedance integral (EII) and volume of inverted impedance (VII) ratios, have shown strong correlations with bolus transit. This study compared the EII and VII ratios as diagnostic tools for NOD.We analyzed 36 participants (12 patients with achalasia, 12 patients with NOD [7 with normal motility and 5 with ineffective esophageal motility], and 12 asymptomatic controls) who underwent HRIM with a maximum of 5 swallows per participant. The EII and VII ratios were calculated as Z2 (post-swallow)/Z1 (pre-swallow). Bolus transit was retrospectively evaluated using transluminal impedance analysis.Both EII and VII ratios could effectively distinguish the achalasia group from the non-achalasia groups (area under the receiver operating characteristic curve [AUROC]: 0.83 for VII vs. 0.80 for EII; p = 0.73). However, the VII ratio was significantly better in discriminating asymptomatic controls from patients with dysphagia (NOD + achalasia) (AUROC: 0.81 vs. 0.68; p = 0.01). Moreover, the VII ratio was better in discriminating asymptomatic controls from patients with NOD (AUROC: 0.68 vs. 0.51; p = 0.06). In repeated swallows, the VII ratio was consistently the lowest in controls and the highest in patients with achalasia, whereas the EII ratio did not show a consistent pattern.The VII ratio was more reliable than the EII ratio for describing bolus transit and distinguishing patients with NOD from asymptomatic controls, even during repeated measures of subsequent swallows.

Helicobacter pylori deregulates the genes that control homeostasis between apoptosis and cell proliferation of gastric epithelial cells. Nuclear factor-kappaB (NF-kappaB) has an important role in H. pylori-induced apoptosis in gastric epithelial cells. The peroxisome proliferator-activated receptor-gamma ligand 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) regulates growth and the signaling cascade in H. pylori-infected gastric epithelial cells. In the present study, we determined whether 15d-PGJ(2) inhibits apoptosis by regulating apoptotic gene expression and NF-kappaB activation in gastric epithelial cells infected with CagA+, VacA+H. pylori in a Korean isolate (HP99). 15d-PGJ(2) was found to inhibit H. pylori-induced DNA fragmentation and cell death. 15d-PGJ(2) induced downregulation of proapoptotic Bax and upregulation of antiapoptotic Bcl-2 as well as suppression of NF-kappaB activation caused by H. pylori in gastric epithelial cells. The results suggest that 15d-PGJ(2) inhibits apoptotic cell death by inhibiting NF-kappaB activation and apoptotic gene expression in gastric epithelial cells.

Our previous studies show that Helicobacter pylori (H. pylori) induces oxidative stress and the expression of proinflammatory cytokines in gastric epithelial cells. H. pylori induces the expression of molecular chaperones and proteins involved in protein-folding machinery as a defense mechanism against cellular stress. The suppressors of cytokine signaling (SOCS) are known as negative regulators of major immune signal pathways. The purpose of this article is to determine whether H. pylori in a Korean isolate (HP99) induces the expression of SOCS in rat gastric mucosal RGM-1 cells as a defense mechanism. As a result, HP99 induced SOCS-3 expression time-dependently in RGM-1 cells. SOCS-1 was not expressed while SOCS-2 expression was not changed by HP99 infection in RGM-1 cells. SOCS-3 might have a defensive role in H. pylori-infected gastric mucosal cells. Further study by manipulating SOCS-3 gene should be performed to investigate the physiological meaning of SOCS-3 induced by H. pylori in gastric mucosal cells.