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Background: Esophageal cancer has a high incidence and one of the highest mortality rates worldwide. There are few studies on the effects of sevoflurane on postoperative metastasis and recurrence of esophageal cancer. This study aimed to investigate the effect of sevoflurane on the progression of esophageal cancer and the underlying mechanism of the sensitivity to cisplatin., Methods: We used the esophageal squamous cell carcinoma (ESCC) line EC109 and esophageal adenocarcinoma (EADC) line SKGT-4. Cell proliferation and stemness potential were determined by MTT assay and sphere-forming assays, respectively. The protein expression of (sex determining region Y)-box 2 (SOX2) and octamer-binding transcription factor 4 (OCT4) was determined by western blot. Cell migration and invasion ability were separately determined by scratch assay and transwell assays, respectively. The distribution of cell cycle and apoptosis were detected by flow cytometry, and the levels of lactate dehydrogenase (LDH) were measured by the enzyme-linked immunosorbent assay (ELISA)., Results: In the SKGT-4 cells, exposure to sevoflurane inhibited proliferation, increased the migration and invasion potential, increased the number of cells in S phase, promoted self-renewal ability, and up-regulated the expression of SOX2 and OCT4 compared with control cells. Compared with the cisplatin treated group, treatment with sevoflurane plus cisplatin reduced the level of LDH and inhibited apoptosis in the SKGT-4 cells. However, sevoflurane did not affect EC109 cells., Conclusions: Long-term exposure to sevoflurane inhibited the proliferation, increased migration and invasion capacity, and decreased the sensitivity to cisplatin in EADC by promoting stemness. However, sevoflurane had no effect on the behavior of ESCC., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tcr.amegroups.com/article/view/10.21037/tcr-21-2404/coif). The authors have no conflicts of interest to declare., (2022 Translational Cancer Research. All rights reserved.)

Normal temperature catalytic ozonation is an effective method for the removal of volatile organic compounds (VOCs). A series of TiO 2 -supported noble metal catalysts were synthesized by a facile impregnation method. The as-prepared catalysts were evaluated for the catalytic oxidation of toluene. It was determined that the 1 wt%Pt/TiO 2 exhibited outstanding performance that 65% conversion of toluene was achieved with the space velocity of 30,000 h -1 even at room temperature (25°C). The structure-activity relationship of various catalysts was investigated via BET, XRD, SEM, TEM as well as XPS. The results indicated that the uniform dispersion of Pt nanoparticles, abundant surface adsorbed oxygen species as well as the strong interaction between Pt and TiO 2 favoured toluene degradation at normal temperature. Based on FT-IR, a simplified reaction scheme was proposed: toluene was first oxidized to benzoate species then alcohol species, ketones, carboxyl acids, which was finally degraded into CO 2 and H 2 O. The low activation energy of 1 wt%Pt/TiO 2 determined to be 47 kJ mol -1 also benefited for toluene degradation at ambient temperature.

Normal temperature catalytic ozonation (NTCO) is a promising yet challenging method for the removal of volatile organic compounds (VOCs) because of limited activity of the catalysts at ambient temperature. Here, we report a series of Pt/FeO x catalysts prepared by the co-precipitation method for NTCO of gaseous methanol. All samples were found to be active and among them, the Pt/FeO x -400 (calcined at 400 °C) catalyst with a Pt cluster loading of 0.2% exhibited the highest activity, able to completely convert methanol into CO 2 and H 2 O at 30 °C. Extensive experimental research suggested that the superior catalytic activity could be attributed to the highly dispersed Pt clusters and an appropriate molar ratio of Pt 0 /Pt 2+ . Furthermore, electron paramagnetic resonance and density functional theory computational studies revealed the mechanism that the Pt/FeO x -400 catalyst could activate O 3 and water effectively to produce hydroxyl radicals responsible for the catalytic oxidation of methanol. The findings of this work may foster the development of technologies for normal temperature abatement of VOCs with low energy consumption.

A full scale snow melting system with heat pipe technology is built in this work, which avoids the negative effects on concrete structure and environment caused by traditional deicing chemicals. The snow melting, ice-freezing performance and temperature distribution characteristics of heat pipe concrete runway were discussed by the outdoor experiments. The results show that the temperature of the concrete pavement is greatly improved with the heat pipe system. The environment temperature and embedded depth of heat pipe play a dominant role among the decision variables of the snow melting system. Heat pipe snow melting pavement melts the snow completely and avoids freezing at any time when the environment temperature is below freezing point, which is secure enough for planes take-off and landing. Besides, the exportation and recovery of geothermal energy indicate that this system can run for a long time. This paper will be useful for the design and application of the heat pipe used in the runway snow melting.

Aminopeptidase N (APN) belonging to zinc-dependent metalloproteinase, not only catalyzes protein proteolytic process, but also is involved in the pathogenic process as the receptor of pathogenic toxin. In Bombyx mori, APN gene family consists of 16 members, of which BmAPN4 binds trypsin-activated parasporal crystal (PC) toxin isolated from Bacillus bombysepticus (Bb). In order to verify whether or not other APNs interact with PC toxin during the pathogenesis of Bb, we cloned BmAPN5, a member of aminopeptidase family, from the silkworm midgut. The full length of BmAPN5 is 3313 bp, encoding 953 amino acids, containing a zinc peptidase_M1 and ERAP1_C domains. A recombinant GST-BmAPN5 was purified by a prokaryotic expression system. Far-Western blotting, co-immunoprecipitation and ELISA. Binding saturation assays demonstrated that PC after activated by trypsin could be bound by BmAPN5. Additionally, cytotoxic activity of trypsin-activated PC in Sf9 cells transfected with BmAPN5 showed that cells exhibited dramatic cytological changes, including swelling and lysis, revealing BmAPN5 serves as a functional receptor that participates in Bb and PC pathogenicity. These provide some clues for further exploring the pathogenesis relationships of Bb and host.

The physiological level of nitric oxide (NO) released by brain microvascular endothelial cells (BMECs) at normoxia can block the degradation of hypoxia-inducible factor-1α (HIF-1α) in astrocytes and initiate the compensatory response to hypoxia. However, it is unclear whether this occurs at mild hypoxia. This study was to investigate the expression of HIF-1α, VEGF and LDHA and the lactic acid production in astrocytes with or without co-culture with BMECs after mild hypoxia exposure. During mild hypoxia (5% O 2 ), exogenous NO blocked the degradation of HIF-1α in astrocytes but up-regulated the transcription of VEGF and LDHA, accompanied by elevated expression of VEGF protein and increased production of lactic acid. This was further confirmed by silencing of HIF-1α expression in astrocytes. In astrocytes co-cultured with primary rat BMEC under mild hypoxia, NO was released by the BMECs and prevented the degradation of HIF-1α in astrocytes, leading to the up-regulated mRNA expression of VEGF and LDHA, elevated VEGF protein expression and increased production of lactic acid. In BMECs, NO was derived from intracellular eNOS. Based on these findings, we hypothesize that, under mild hypoxia, even though astrocytes do not respond to hypoxia, NO produced by BMECs may transmit a hypoxia signal to astrocytes, triggering their adaptive response via HIF-1α.

The p38 mitogen-activated protein kinase (MAPK) plays a key role in lipopolysaccharide (LPS)-induced signal transduction pathways that lead to inflammatory cytokine synthesis in macrophages; however, whether the inhibition of p38 MAPK regulates LPS-induced inflammatory cytokine expression in different types of macrophages remains the subject of debate. Herein, we assessed whether the inhibition of p38 MAPK by SB203580 regulates LPS-induced expression of the inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in RAW264.7 and resident peritoneal macrophages. Lipopolysaccharide stimulation of RAW264.7 macrophages or mouse resident peritoneal macrophages significantly increased TNF-α and IL-6 production. The addition of SB203580 to cultures dramatically blocked LPS-induced TNF-α production in RAW264.7 and mouse resident peritoneal macrophages, and dramatically blocked LPS-induced IL-6 production in RAW264.7 macrophages, but not in mouse resident peritoneal macrophages. Additionally, high concentrations of SB203580 resulted in increased IL-6 production. However, LPS-stimulation significantly up-regulated the mRNA transcript levels of TNF-α and IL-6 in RAW264.7 and mouse resident peritoneal macrophages, whereas pretreatment with SB203580 dramatically down-regulated LPS-induced mRNA transcript levels of TNF-α and IL-6 in these cells. Our data show that SB203580 differentially modulates LPS-induced production of the inflammatory cytokine IL-6 in two different sources of macrophages, and that this course of regulation occurs at the IL-6 mRNA post-transcriptional stage.

It is still challenging to prevent and treat respiratory infectious diseases. One critical step in the successful treatment of respiratory infections is rapid diagnosis by identifying the causative microorganisms in a timely fashion. However, traditional methods for identification of causative agents could not satisfy the need for rapid and accurate testing due to the limitations of technology-used. In recent years, matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) has been validated and used for rapid identification of microorganism and for potential discovery of diseases associated biomarkers. We reviewed recent advances of MALDI-TOF-MS as the laboratory diagnostic tool for the rapid laboratory diagnosis of microorganisms associated with respiratory infectious diseases, with the focus on rapid identification of pathogenic bacteria and molecular markers discovery using MALDI-TOF-MS. With the advanced technologies such as MALDI-TOF, early and targeted therapies based on rapid identification of pathogens and could lead to quick and effective treatment of respiratory infections and better patient management.