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The application of sludge biochar (SC) materials as efficient catalysts for organic pollutants mineralization via advanced oxidation process meets the good strategy of "make waste profitable". The catalytic oxidations of methyl orange (MO) and pyrene by oxalic acid modified sludge biochar (SC-OA) with and without H 2 O 2 were carried out. The analysis of Fourier transform infrared (FT-IR), X-ray photoelectron spectroscopy (XPS), electronic paramagnetic resonance spectrometer (EPR) and free radical quenching experiment were performed and the definite relationships between persistent free radicals (PFRs) type and specific reactive oxygen species (ROS) were made clear. It is suggested for the first time that carbon-centered type PFRs in SC-OA without H 2 O 2 could form O 2 •- and •OH from COOH groups, while oxygen-centered type PFRs induced H 2 O 2 to produce •OH. The degradation intermediates of MO and pyrene were identified and the transformation pathways were proposed. SC-OA, possessing good sustainable utilization and clean catalytic property, is expected to be popularized and applied in the mineralization of organic pollutants, especially in the in-situ remediation of contaminated soil where is no continuous supply of H 2 O 2. It is known that the g-factors for oxygen-centered radicals are larger than 2.0040, while g-factors less than 2.0030 correspond to carbon-centered radicals. As shown in Fig. 4a, the g-factors for SC, SC-OA, and SC-OA deg were 2.1326, 1.9914, and 2.1330, indicating that carbon-centered PFRs played a key role in the catalytic degradation of MO. From the above results, we can speculate that SC has the intrinsic oxygen-centered type PFRs, and OA monoanion on the SC-OA can convert to carbon-centered PFRs (SC–OH/HOOC•) under the activation of the oxygen-centered PFRs followed by radical decarboxylation to give CO 2 and formate. Then, SC-OH/HOOC• stimulates the generation of ROS. [Display omitted] • The relationships of PFRs type and ROS generation was made clear. • Carbon-centered type PFRs in SC-OA prefer to form O 2.•- and •OH without H 2 O 2. • Oxygen-centered type PFRs in SC contribute to induce H 2 O 2 to produce.•OH. • SC-OA possess good sustainable utilization and clean catalytic property. [ABSTRACT FROM AUTHOR]

• Protective autophagy induced by DDP decreases chemosensitivity in GC cells. • MGMT inhibited ATG4B to repress autophagy. • Inhibition of autophagy enhanced the chemosensitivity to DDP in GC xenograft model. • High MGMT expression and low ATG4B expression are significantly correlated with survival of GC. Cisplatin (DDP) is the first-line drug for the treatment of gastric cancer (GC). However, DDP resistance is common. Autophagy, which is closely related to chemoresistance, is a process of resolving and recycling proteins and damaged cellular organs. Additionally, O-6-methylguanine-DNA methyltransferase (MGMT) is responsible for alkylating drug resistance. However, the relationship between autophagy and MGMT in response to DDP in GC is still unknown. In the present study, we determined that autophagy induced by DDP decreases chemosensitivity in GC cell lines. DDP may have induced autophagy in GC by inhibiting MGMT to increase autophagy-related gene (ATG) 4B. Inhibition of MGMT-mediated ATG4B suppression resulted in autophagy induction and DDP resistance. In vivo , combined DDP and autophagy inhibitor chloroquine (CQ) enhanced the anti-tumor effect of DDP; additionally, the negative correlation of MGMT and ATG4B was confirmed. High expression of MGMT and low expression of ATG4B were significantly correlated with favorable five-year survival rate (P < 0.05) in 66 clinicopathologically characterized GC cases. Our study demonstrate that DDP inhibits MGMT-mediated autophagy suppression to decrease chemosensitivity in GC, which provides a novel therapeutic strategy to promote DDP chemosensitivity in GC. [ABSTRACT FROM AUTHOR]

Abstract: Nitric oxide (NO) aided Si0.85Ge0.15 wet-oxynitridation has been performed at 400–700 °C, while the wet-NO feed gas was preheated to higher temperatures before entering the reaction zone. X-ray photoelectron spectroscopy (XPS) and secondary ion mass spectroscopy data suggests that both nitrogen and oxygen incorporation increases within the dielectric bulk with increasing wet-oxynitridation temperature, while there is no apparent germanium segregation towards the dielectric/substrate interface at all temperatures studied. Moreover, angle-resolved XPS analysis suggests that wet-oxynitridation at temperatures higher than 600 °C volatilizes some germanium oxide from the surface region, while silicon monoxide is outgassed from the dielectric bulk and accumulates near the surface. Nitrogen incorporation is found to hinder germanium segregation. Z-contrast imaging with scanning transmission electron microscopy shows that oxynitrides grown in wet-NO have sharp interfaces with bulk Si0.85Ge0.15, while the roughness of the dielectric/Si0.85Ge0.15 substrate interface is less than 2 Å. These results are discussed in the context of an overall mechanism of SiGe wet-oxynitridation. [Copyright &y& Elsevier]

The gut microbiota forms a symbiotic relationship with the host and benefits the body in many critical aspects of life. However, immune system defects, alterations in the gut microbiota and environmental changes can destroy this symbiotic relationship and may lead to diseases, including cancer. Due to the anatomic and functional connection of the gut and liver, increasing studies show the important role of the gut microbiota in the carcinogenesis of hepatocellular carcinoma (HCC). In this manuscript, we review the available evidence and analyze some potential mechanisms of the gut microbiota, including bacterial dysbiosis, lipopolysaccharide (LPS), and genotoxins, in the progression and promotion of HCC. Furthermore, we discuss the possible therapeutic applications of probiotics, chemotherapy modulation, immunotherapy, targeted drugs and fecal microbiota transplantation (FMT) in targeting the gut microbiota. [ABSTRACT FROM AUTHOR]

Immune checkpoint inhibitors against PD-1/PD-L1 yield improved survival rates of KRAS-mutant NSCLC patients, who conferred a poor prognosis without effective targeted therapy until now. Yet, the underlying association between KRAS mutations and immune responses remains unclear. We performed an integrated analysis of the data from publicly available repositories and from clinical center cohorts to explore the association between KRAS mutation status and tumor immunity-associated features, including PD-L1 expression, CD8+ tumor-infiltrating lymphocytes (TILs) and tumor mutational burden (TMB). Our results revealed that KRAS mutations are correlated with an inflammatory tumor microenvironment and tumor immunogenicity, resulting in superior patient response to PD-1/PD-L1 inhibitors. Meanwhile, three-pool analysis further confirmed that KRAS-mutant NSCLC patients show remarkable clinical benefit from anti-PD-1/PD-L1 immunotherapy. In addition, a KRAS-mutant lung adenocarcinoma mouse model was established to estimate the relative efficacy of anti-PD-L1 monoclonal antibody monotherapy or combination treatment with docetaxel versus docetaxel alone. Most surprisingly, we found that PD-L1 blockade combined with docetaxel did not promote an anti-tumor response. These findings uncover that PD-1/PD-L1 blockade monotherapy may be the optimal therapeutic schedule in NSCLC patients harboring KRAS mutations. [ABSTRACT FROM AUTHOR]

Interferons (IFNs) play crucial roles in the development and treatment of cancer. Long non-coding RNAs (lncRNAs) are emerging molecules involved in cancer progression. Here, we identified and characterized an IFN-inducible nuclear lncRNA IRF1-AS (Interferon Regulatory Factor 1 Antisense RNA) which was positively correlated with IRF1 expression. IFNs upregulate IRF1-AS via the JAK-STAT pathway. Knockdown and overexpression of IRF1-AS revealed that IRF1-AS inhibits oesophageal squamous cell carcinoma (ESCC) proliferation and promotes apoptosis in vitro and in vivo. Mechanistically, IRF1-AS activates IRF1 (Interferon Regulatory Factor 1) transcription through interacting with ILF3 (Interleukin Enhancer Binding Factor 3) and DHX9 (DExH-Box Helicase 9). In turn, IRF1 binds to the IRF1-AS promoter directly and activates IRF1-AS transcription. Global analysis of IRF1-AS-regulated genes indicated that IRF1-AS activates the IFN response in vitro and in vivo. IRF1 knockdown in IRF1-AS-overexpressing cells abolished the antiproliferative effect and activation of the IFN response. Furthermore, IRF1-AS was downregulated in ESCC tissues, and low expression correlated with poor prognosis. In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) play critical roles in multiple cellular processes in non-small cell lung cancer (NSCLC); however, the involvement of lncRNAs in the transforming growth factor-beta (TGFβ) signaling pathway, the critical tumor cell epithelial-mesenchymal transition (EMT) and metastasis pathway, remains poorly understood. To address this issue, we compared the lncRNAs expression patterns of NSCLC cells treated with and without TGFβ1 treatment. We observed that one of the most prominent hits, TGFβ-induced lncRNA (TBILA), promoted NSCLC progression and was upregulated in tumor tissues. Upregulated TBILA promotes human germinal center-associated lymphoma (HGAL) expression by binding to the Smad transcription factor complex, thereby enhancing RhoA activation. In addition, TBILA induces the S100A7-c-Jun activation domain-binding protein 1 (JAB1) pathway by binding to nuclear S100A7 and enhances pro-survival pathways in NSCLC. These findings have provided us with a new perspective regarding the regulation of the TGFβ signaling pathway in NSCLC and suggest that the lncRNA TBILA can serve as a target for anticancer therapies. [ABSTRACT FROM AUTHOR]