Esophageal motility disorders were re-defined when high-resolution manometry was employed to better understand their pathogenesis. Newly developed parameters including integrated relaxation pressure (IRP), distal contractile integral, and distal latency showed better diagnostic yield compared with previously used conventional parameters. Therefore, Chicago classification was formulated, and its diagnostic cascade begins by assessing the IRP value. However, IRP showed limitation due to its inconsistency, and other studies have tried to overcome this. Recent studies showed that provocative tests, supplementing the conventional esophageal manometry protocol, have improved the diagnostic yield of the esophageal motility disorders. Therefore, position change from supine to upright, solid or semi-solid swallowing, multiple rapid swallows, and the rapid drink challenge were newly added to the manometry protocol in the revised Chicago classification version 4.0. Impedance planimetry enables measurement of bag cross-sectional area at various locations. The functional lumen imaging probe (FLIP) has been applied to assess luminal distensibility. This probe can also measure pressure, serial cross-sectional areas, and tension-strain relationship. The esophagogastric junction’s distensibility is decreased in achalasia. Therefore, EndoFLIP can be used to assess contractility and distensibility of the esophagus in the patients with achalasia, including repetitive antegrade or retrograde contractions. EndoFLIP can detect achalasia patients with relatively low IRP, which was difficult to diagnose using the current high-resolution manometry. EndoFLIP also provides information on the contractile activity and distensibility of the esophageal body in patients with achalasia. The use of provocative tests, newly added in Chicago classification 4.0 version, and EndoFLIP can expand understanding of esophageal motility disorders.

Despite advancements in endoscopic technology and drug therapy, the high mortality and rebleeding rates associated with hemorrhagic peptic ulcers remain a concern. Although further research is needed to validate contributing factors, I recommend use of the Rockall score to predict the rebleeding risk in patients with peptic ulcers. Greater caution should be exercised, particularly in hospitalized patients, those who have undergone pancreatic surgery, and those with bleeding due to Dieulafoy’s lesions. Delaying resumption of an oral diet for at least 24 hours after endoscopic bleeding control is also advisable.

Despite advancements in endoscopic technology and drug therapy, the high mortality and rebleeding rates associated with hemorrhagic peptic ulcers remain a concern. Although further research is needed to validate contributing factors, I recommend use of the Rockall score to predict the rebleeding risk in patients with peptic ulcers. Greater caution should be exercised, particularly in hospitalized patients, those who have undergone pancreatic surgery, and those with bleeding due to Dieulafoy’s lesions. Delaying resumption of an oral diet for at least 24 hours after endoscopic bleeding control is also advisable.

Despite advancements in endoscopic technology and drug therapy, the high mortality and rebleeding rates associated with hemorrhagic peptic ulcers remain a concern. Although further research is needed to validate contributing factors, I recommend use of the Rockall score to predict the rebleeding risk in patients with peptic ulcers. Greater caution should be exercised, particularly in hospitalized patients, those who have undergone pancreatic surgery, and those with bleeding due to Dieulafoy’s lesions. Delaying resumption of an oral diet for at least 24 hours after endoscopic bleeding control is also advisable.

Despite advancements in endoscopic technology and drug therapy, the high mortality and rebleeding rates associated with hemorrhagic peptic ulcers remain a concern. Although further research is needed to validate contributing factors, I recommend use of the Rockall score to predict the rebleeding risk in patients with peptic ulcers. Greater caution should be exercised, particularly in hospitalized patients, those who have undergone pancreatic surgery, and those with bleeding due to Dieulafoy’s lesions. Delaying resumption of an oral diet for at least 24 hours after endoscopic bleeding control is also advisable.

Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-kappaB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present study is to determine whether H. pylori-induced activation of NF-kappaB and the expression of interleukin-8 (IL-8) are mediated by the activation of Jak1/Stat3 in gastric epithelial (AGS) cells. Thus, gastric epithelial AGS cells were infected with H. pylori in Korean isolates (HP99) at bacterium/cell ratio of 300:1, and the level of IL-8 in the medium was determined by enzyme-linked immonosorbent assay. Phospho-specific and total forms of Jak1/Stat3 and IkappaBalpha were assessed by Western blot analysis, and NF-kappaB activation was determined by electrophoretic mobility shift assay. The results showed that H. pylori induced the activation of Jak1/Stat3 and IL-8 production, which was inhibited by a Jak/Stat3 specific inhibitor AG490 in AGS cells in a dose-dependent manner. H. pylori-induced activation of NF-kappaB, determined by phosphorylation of IkappaBalpha and NF-kappaB-DNA binding activity, were inhibited by AG490. In conclusion, Jak1/Stat3 activation may mediate the activation of NF-kappaB and the expression of IL-8 in H. pylori-infected AGS cells. Inhibition of Jak1/Stat3 may be beneficial for the treatment of H. pylori-induced gastric inflammation, since the activation of NF-kappaB is inhibited and inflammatory cytokine expression is suppressed.
Blotting, Western ; DNA, Bacterial/analysis/genetics ; Epithelial Cells/metabolism ; Gastric Mucosa/drug effects/*immunology/microbiology ; Gene Expression Regulation/drug effects/*immunology ; Gene Expression Regulation, Bacterial ; Helicobacter Infections/immunology/*metabolism ; Helicobacter pylori/genetics/pathogenicity/*physiology ; Humans ; Interleukin-8/genetics/*metabolism ; Janus Kinase 1 ; NF-kappa B/biosynthesis/*metabolism ; Phosphorylation ; RNA, Messenger/metabolism ; STAT3 Transcription Factor ; Signal Transduction/genetics