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Benefiting from similar hydrogen bonding energy to Pt and much lower price compare with Pt, Ru based catalysts are promising candidates for electrocatalytic hydrogen evolution reaction (HER). The catalytic activity of Ru nanoparticles can be enhanced through improving their dispersion by using different supports, and the strong metal supports interaction can further regulate their catalytic performance. In addition, single-atom catalysts (SACs) with almost 100% atomic utilization attract great attention and the coordinative atmosphere of single atoms can be adjusted by supports. Moreover, the syngenetic effects of nanoparticles and single atoms can further improve the catalytic performance of Ru based catalysts. In this review, the progress of Ru based HER electrocatalysts are summarized according to their existing forms, including nanoparticles (NPs), single atoms (SAs) and the combination of both NPs and SAs. The common supports such as carbon materials, metal oxides, metal phosphides and metal sulfides are classified to clarify the metal supports interaction and coordinative atmosphere of Ru active centers. Especially, the possible catalytic mechanisms and the reasons for the improved catalytic performance are discussed from both experimental results and theoretical calculations. Finally, some challenges and opportunities are prospected to facilitate the development of Ru based catalysts for HER., (© 2024 Wiley‐VCH GmbH.)

Introduction: Sepsis and septic shock are significant contributors to the development of acute kidney injury (AKI) in critically ill patients. This study aimed to elucidate the role and mechanism of microRNA-223-3p in sepsis-associated AKI (SA-AKI)., Methods: Bioinformatics methods were used to analyze the expression of microRNA-223-3p in sepsis patients, its correlation with inflammatory cytokines, and to predict the binding site of microRNA-223-3p with SGK1. The binding relationship between microRNA-223-3p and SGK1 was validated using a dual-luciferase reporter gene assay. The expression of microRNA-223-3p was assayed using qPCR in patient serum or lipopolysaccharide (LPS)-treated HK-2 cells. Cell apoptosis; expression of Bax, Bcl-2, cleaved caspase-3; and levels of TNF-α, IL-1β, and IL-6 were measured using TUNEL assay, Western blot (WB), and ELISA, respectively. SGK1 expression of HK-2 cells with different treatments was detected using qPCR and WB., Results: The expression of microRNA-223-3p was found to be upregulated in sepsis patients and HK-2 cells treated with LPS. Furthermore, microRNA-223-3p promoted apoptosis and inflammation in LPS-induced HK-2 cells. This promotion was mediated by the negative regulation of SGK1 by microRNA-223-3p., Conclusion: The microRNA-223-3p was found to regulate SGK1 and promote apoptosis and inflammation in LPS-induced HK-2 cells. Our study has elucidated the mechanism of microRNA-223-3p in SA-AKI, providing a potential target for sepsis treatment., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

It has been reported that HMGB1 participated in various types of lung injury. In this study, we explored whether blocking HMGB1 has a preventive effect on the early radiation-induced lung injury and investigate the mechanism. Mice model of radiation-induced lung injury were accomplished by a single dose irradiation (15 Gy) to the whole thorax. Irradiated mice were treated with HMGB1-neutralizing antibody intraperitoneally dosed 10 μg, 50 μg, 100 μg/mouse respectively and were sacrificed after one week post-irradiation. Lung tissue slices were stained by H&E, and alveolitis was quantified by Szapiel scoring system. The level of cytokines TNF-γ in bronchoalveolar lavage fluid was detected by ELISA method. And p65NF-κB, p50NF-κB protein expression in mice lung tissues was detected by Western blot analysis. The results showed that blocking HMGB1 inhibited the inflammatory response, and thereby decreased the degree of alveolitis of irradiated lung tissue. In addition, HMGB1 antagonist can restrain the expression of type Th2 or Th17 derived inflammatory cytokines TNF-α, IL-6 and IL-17A, promote the expression of Th1 type cytokines INF-γ, and inhibit p65 NF-κB but promote p50 NF-κB activation, which promoted the resolution of the radiation-induced inflammatory response. In conclusion, blocking HMGB1 can reduce the degree of early radiation-induced lung injury, and its mechanism may be related to the promotion of p50NF-κB activation and its downstream molecules expression. Inhibiting HMGB1 may be a new target to deal with early radiation-induced lung injury.

The prognostic value of the HPV status in ESCC is much controversial, this study aimed to determine the prognostic importance of high-risk HPV and p16 in patients with ESCC. A total of 105 consecutive patients who underwent esophagectomy in 2008 were included in this study. All specimens with ESCC were tested by in situ hybridization for HPV16/18 and immunohistochemistry for p16 expression. Kappa values were calculated using Cohen's kappa test. The 5-year overall survival (OS) and progression-free survival (PFS) were calculated in relation to the two markers and the Cox proportional hazards model was used to determine the hazard ratio (HR) of variables. Thirty-nine (37.1%) of 105 were p16-positive, and HPV was detected in 29 of the 105 patients (27.6%) with ESCC. P16 was detected in 25 of the 29 patients (86.2%) who were HPV-positive, and only 14 of 76 patients (18.4%) who were HPV-negative (P < 0.001). Cohen's kappa coefficient revealed an agreement in two researchers (kappa = 0.61). The 5-year OS rate and PFS rate in the p16-positive group were 64.1% and 58.7%, respectively, and the rates in the p16-negative group were 45.5%, 37.9%, respectively. The difference of survival rate between the two groups remained statistically significant. P16-positive patients had better 5-year rates of OS and PFS than p16-negative group (P = 0.02 and P = 0.007 by the Log-rank test, respectively). Using HPV status as a stratification factor, we found differences in OS and PFS that were consistent with those based on p16 expression. P16 is a very good marker of HPV infection for ESCC. HPV-positive or p16-positive ESCC is a distinct entity with a favorable prognosis compared with HPV-negative or p16-negative ESCC.