Thanks to more and more gamma-ray bursts with measured redshift and extended emission detected by the recent space telescopes, it is urgent and possible to check whether those previous energy correlations still satisfy the particular sample involving only the bursts accompanied by tail radiations. Using 20 long and 22 short bursts with extended emission, we find that the popular γ -ray energy correlations of the intrinsic peak energy versus the isotropic energy (Amati relation) and the intrinsic peak energy versus the peak luminosity (Yonetoku relation) do exist in both short and long bursts. However, it is much better if these gamma-ray bursts with extended emissions are reclassified into two subgroups of E-I and E-II that make the above energy correlations more tight. As proposed by Zhang et al., the energy correlations can be utilized to distinguish these kinds of gamma-ray bursts in the plane of bolometric fluence versus peak energy as well. Interestingly, the peculiar short GRB 170817A belongs to the E-I group in the fluence versus peak energy plane, but it is an outlier of both the Amati and Yonetoku relations even though the off-axis effect has been corrected. Furthermore, we compare the radiation features between the extended emissions and the prompt gamma-rays in order to search for their possible connections. Taking into account all these factors, we conclude that gamma-ray bursts with extended emission are still required to model with dichotomic groups, namely E-I and E-II classes, which hint that they might have different origins.

Helicobacter pylori (H. pylori) is a well-known pathogen associated with chronic gastric infection, progressing from gastritis to gastric adenocarcinoma, but the dynamic phenotypic and molecular characteristics of gastric epithelial cells during sustained infection remain unclear. We established a chronic infection model using the human gastric epithelial cell line GES-1, exposed to H. pylori or its lysate across 30 generations, dynamically assessing cell proliferation, migration, invasion, apoptosis, autophagy, and epithelial–mesenchymal transition (EMT) markers, with RNA sequencing for transcriptomic changes and a Mongolian gerbil model to validate chronic pathological progression. Acute H. pylori exposure induced pronounced morphological changes; suppressed proliferation, migration, and invasion; triggered apoptosis; and blocked autophagic flux, while long-term stimulation reversed these effects. EMT markers showed progressive loss of epithelial characteristics with chronic infection. RNA sequencing revealed a dynamic shift from inflammation-driven apoptosis to adaptive survival mechanisms. In vivo, prolonged infection induced dynamic TLR expression alongside progressive gastric pathology, including atrophy and dysplasia. Our study provides new molecular evidence for dynamic cellular and immunological adaptations of gastric epithelial cells under chronic H. pylori infection, highlighting critical intervention windows for preventing gastric carcinogenesis.