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Hepatocellular carcinoma (HCC) is one of the deadliest cancers. The prevention and therapy for this deadly disease remain a global medical challenge. In this study, we investigated the effect of pantoprazole (PPZ) on the carcinogenesis and growth of HCC. Both diethylnitrosamine (DEN) plus CCl4‐induced and DEN plus high fat diet (HFD)‐induced HCC models in mice were established. Cytokines and cell proliferation‐associated gene in the liver tissues of mice and HCC cells were analyzed. Cellular glycolysis and Na+/H+ exchange activity were measured. The preventive administration of pantoprazole (PPZ) at a clinically relevant low dose markedly suppressed HCC carcinogenesis in both DEN plus CCl4‐induced and HFD‐induced murine HCC models, whereas the therapeutic administration of PPZ at the dose suppressed the growth of HCC. In the liver tissues of PPZ‐treated mice, inflammatory cytokines, IL1, CXCL1, CXCL5, CXCL9, CXCL10, CCL2, CCL5, CCL6, CCL7, CCL20, and CCL22, were reduced. The administration of CXCL1, CXCL5, CCL2, or CCL20 all reversed PPZ‐suppressed DEN plus CCL4‐induced HCC carcinogenesis in mice. PPZ inhibited the expressions of CCNA2, CCNB2, CCNE2, CDC25C, CDCA5, CDK1, CDK2, TOP2A, TTK, AURKA, and BIRC5 in HCC cells. Further results showed that PPZ reduced the production of these inflammatory cytokines and the expression of these cell proliferation‐associated genes through the inhibition of glycolysis and Na+/H+ exchange. In conclusion, PPZ suppresses the carcinogenesis and growth of HCC, which is related to inhibiting the production of inflammatory cytokines and the expression of cell proliferation‐associated genes in the liver through the inhibition of glycolysis and Na+/H+ exchange. [ABSTRACT FROM AUTHOR]

Low-damage plasma oxidation treatment for AlN/GaN high-electron-mobility transistors (HEMTs) was developed in this letter, with which high-performance enhancement-mode (E-mode) AlON/AlN/GaN HEMTs were demonstrated. After removal of in situ SiN cap layer within gate area, remote plasma oxidation (RPO) treatment of 4.9nm AlN barrier layer at 300 °C leads to formation of AlON insulator layer and effective depletion of 2-D electron gas channel, without etch-induced damage or serious interfacial issues compared with the commonly used gate- recess metal-insulator-semiconductor HEMTs. Thanks to the low-damage RPO treatment, the achieved E-mode HEMTs with threshold voltage of 0.4 V exhibit quite a small loss of output current (7.8%) compared with the depletion-mode devices. In addition, the AlON gate insulator layer results in a remarkable increase in breakdown voltage of devices from 20 V to 74 V, which benefits the high-voltage operation of AlN/GaN technology. Further investigation shows that the oxidation process of AlN barrier tends to be saturated with treatment time increasing, providing a promising solution to the high-performance E-mode operation of scaled GaN-based HEMTs in RF applications. [ABSTRACT FROM AUTHOR]

AlGaN/GaN high-electron-mobility transistors (HEMTs) with Si-rich SiN/Si3N4 bilayer passivation were studied in this article. The use of a Si-rich SiN interlayer leads to improved channel transport property, current collapse, power performance, and temperature-dependent stability. Devices without Si-rich SiN interlayer passivation exhibit an increase in the gate leakage current by over three orders of magnitudes with temperature increasing from 300 to 420 K, leading to an increase in a current collapse from 9.7% to 24.7%, while the devices with Si-rich SiN passivation exhibit a weak temperature dependence of leakage current and a constant current collapse about 5%. Small signal characterization shows that Si-rich SiN passivation results in a remarkable decrease in the effective gate length by ~15% with temperature up to 420 K. At 17 GHz, devices with Si-rich SiN interlayer passivation exhibit an output power density of 7 W/mm and a peak power-added efficiency (PAE) of 56%. The improved power performance of devices using Si-rich SiN interlayer passivation is attributed to the suppressed current collapse and superior device stability under high channel temperature. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the deadliest cancers. The prevention and therapy for this deadly disease remain a global medical challenge. In this study, we investigated the effect of pantoprazole (PPZ) on the carcinogenesis and growth of HCC. Both diethylnitrosamine (DEN) plus CCl4-induced and DEN plus high fat diet (HFD)-induced HCC models in mice were established. Cytokines and cell proliferation-associated gene in the liver tissues of mice and HCC cells were analyzed. Cellular glycolysis and Na + /H + exchange activity were measured. The preventive administration of pantoprazole (PPZ) at a clinically relevant low dose markedly suppressed HCC carcinogenesis in both DEN plus CCl4-induced and HFD-induced murine HCC models, whereas the therapeutic administration of PPZ at the dose suppressed the growth of HCC. In the liver tissues of PPZ-treated mice, inflammatory cytokines, IL1, CXCL1, CXCL5, CXCL9, CXCL10, CCL2, CCL5, CCL6, CCL7, CCL20, and CCL22, were reduced. The administration of CXCL1, CXCL5, CCL2, or CCL20 all reversed PPZ-suppressed DEN plus CCL4-induced HCC carcinogenesis in mice. PPZ inhibited the expressions of CCNA2, CCNB2, CCNE2, CDC25C, CDCA5, CDK1, CDK2, TOP2A, TTK, AURKA, and BIRC5 in HCC cells. Further results showed that PPZ reduced the production of these inflammatory cytokines and the expression of these cell proliferation-associated genes through the inhibition of glycolysis and Na + /H + exchange. In conclusion, PPZ suppresses the carcinogenesis and growth of HCC, which is related to inhibiting the production of inflammatory cytokines and the expression of cell proliferation-associated genes in the liver through the inhibition of glycolysis and Na + /H + exchange., (© 2024 Wiley Periodicals LLC.)