Tunable terahertz (THz) functional devices have exhibited superior performances due to the use of active materials, such as liquid crystals, graphene, and semiconductors. However, the tunable range of constitutive parameters of materials is still limited, which leads to the low modulation depth of THz devices. Here, we demonstrate a broadband tunable THz absorber based on hybrid vanadium dioxide (VO
2
) metamaterials. Unlike other phase change materials, VO
2
exhibits an insulator-to-metal transition characteristic and the conductivity can be increased by 4–5 orders of magnitude under external stimulus including electric fields, optical, and thermal pumps. Based on the unique transition character of VO
2
, the maximum tunable range of the proposed absorber can be realized from 5% to 100% by an external thermal excitation. Meanwhile, an absorption greater than 80% in a continuous range with a bandwidth about 2.0 THz can be obtained when VO
2
is in its metal phase at high temperature. Furthermore, the absorber is insensitive to the incident angle up to 50° and such a broadband THz absorber can be used in applications including imaging, modulating, cloaking, and so on.
Cellular senescence is a new mechanism for Helicobacter pylori-induced atrophic gastritis, and H pylori promotes senescence through inflammatory C-X-C motif chemokine receptor 2 signaling. Inhibition of C-X-C motif chemokine receptor 2 signaling is a potential therapy to prevent atrophic gastritis and subsequent precancerous lesions. BACKGROUND & AIMS: The association between cellular senescence and Helicobacter pylori-induced atrophic gastritis is not clear. Here, we explore the role of cellular senescence in H pylori-induced atrophic gastritis and the underlying mechanism. METHODS: C57BL/6J mice were infected with H pylori for biological and mechanistic studies in vivo. Gastric precancerous lesions from patients and mouse models were collected and analyzed using SA Q8-b-gal, Sudan Black B, and immunohistochemical staining to analyze senescent cells, signaling pathways, and H pylori infection. Chromatin immunoprecipitation, luciferase reporter assays, and other techniques were used to explore the underlying mechanism in vitro. RESULTS: Gastric mucosa atrophy was highly associated with cellular senescence. H pylori promoted gastric epithelial cell senescence in vitro and in vivo in a manner that depended on C-X-C motif chemokine receptor 2 (CXCR2) signaling. Interestingly, H pylori infection not only up-regulated the expression of CXCR2 ligands, C-X-C motif chemokine ligands 1 and 8, but also transcriptionally up-regulated the expression of CXCR2 via the nuclear factor-kB subunit 1 directly. In addition, CXCR2 formed a positive feedback loop with p53 to continually enhance senescence. Pharmaceutical inhibition of CXCR2 in an H pylori-infected mouse model attenuated mucosal senescence and atrophy, and delayed further precancerous lesion progression. CONCLUSIONS: Our study showed a new mechanism of H pylori-induced atrophic gastritis through CXCR2-mediated cellular senescence. Inhibition of CXCR2 signaling is suggested as a potential preventive therapy for targeting H pylori-induced atrophic gastritis. GEO data set accession numbers: GSE47797 and GSE3556.
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