Microbial fuel cells (MFCs) have received great attention worldwide due to their potential in recovering electrical energy from waste and inexhaustible biomass. Unfortunately, the difficulty of achieving the high power, especially in real samples, remains a bottleneck for their practical applications. Herein, FeS nanoparticles decorated graphene is fabricated via a simple hydrothermal reaction. The FeS nanoparticles decorated graphene anode not only benefits bacterial adhesion and enrichment of electrochemically active Geobacter species on the electrode surface but also promotes efficient extracellular electron transfer, thus giving rise to a fast start-up time of 2 d, an unprecedented power density of 3220 mW m and a remarkable current density of 3.06 A m in the acetate-feeding and mixed bacteria-based MFCs. Most importantly, the FeS nanoparticles decorated graphene anode successfully achieves a power density of 310 mW m with simultaneous removal of 1319 ± 28 mg L chemical oxygen demand in effluents from a beer factory wastewater. The characteristics of improved power generation and enhanced pollutant removal efficiency opens the door toward development of high-performance MFCs via rational anode design for practical application.

Sorafenib is a first-line molecular-target drug for advanced hepatocellular carcinoma (HCC), but its clinical effects are still limited. In this study we identify Quiescin sulfhydryl oxidase 1 (QSOX1) acting as a cellular pro-oxidant, specifically in the context of sorafenib treatment of HCC. QSOX1 disrupts redox homoeostasis and sensitizes HCC cells to oxidative stress by inhibiting activation of the master antioxidant transcription factor NRF2. A negative correlation between QSOX1 and NRF2 expression was validated in tumor tissues from 151 HCC patients. Mechanistically, QSOX1 restrains EGF-induced EGFR activation by promoting ubiquitination-mediated degradation of EGFR and accelerating its intracellular endosomal trafficking, leading to suppression of NRF2 activity. Additionally, QSOX1 potentiates sorafenib-induced ferroptosis by suppressing NRF2 in vitro and in vivo . In conclusion, the data presented identify QSOX1 as a novel candidate target for sorafenib-based combination therapeutic strategies in HCC or other EGFR-dependent tumor types.

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Background Fibrinogen-like protein 1 (FGL1)—Lymphocyte activating gene 3 (LAG-3) pathway is a promising immunotherapeutic target and has synergistic effect with programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1). However, the prognostic significance of FGL1-LAG-3 pathway and the correlation with PD-L1 in hepatocellular carcinoma (HCC) remain unknown. Methods The levels of LAG-3, FGL1, PD-L1 and cytotoxic T (CD8 + T) cells in 143 HCC patients were assessed by multiplex immunofluorescence. Associations between the marker’s expression and clinical significances were studied. Results We found FGL1 and LAG-3 densities were elevated while PD-L1 and CD8 were decreased in HCC tissues compared to adjacent normal liver tissues. High levels of FGL1 were strongly associated with high densities of LAG-3 + cells but not PD-L1. CD8 + T cells densities had positive correlation with PD-L1 levels and negative association with FGL1 expression. Elevated densities of LAG-3 + cells and low levels of CD8 + T cells were correlated with poor disease outcome. Moreover, LAG-3 + cells deteriorated patient stratification based on the abundance of CD8 + T cells. Patients with positive PD-L1 expression on tumor cells (PD-L1 TC + ) tended to have an improved survival than that with negative PD-L1 expression on tumor cells (PD-L1 TC − ). Furthermore, PD-L1 TC − in combination with high densities of LAG-3 + cells showed the worst prognosis, and PD-L1 TC + patients with low densities of LAG-3 + cells had the best prognosis. Conclusions LAG-3, FGL1, PD-L1 and CD8 have distinct tissue distribution and relationships with each other. High levels of LAG-3 + cells and CD8 + T cells represent unfavorable and favorable prognostic biomarkers for HCC respectively.

The overall response rate for anti-PD-1 therapy remains modest in hepatocellular carcinoma (HCC). We found that a combination of interferon alpha (IFN-a) and anti-PD-1-based immunotherapy resulted in enhanced antitumor activity in unresectable HCC patients. In both immunocompetent orthotopic and spontaneous HCC models, IFN-a therapy synergized with anti-PD-1 and the combination treatment led to significant enrichment of cytotoxic CD27+ CD8+ T cells. Mechanistically, IFN-a suppressed HIF1a signaling by inhibiting FosB transcription in HCC cells, resulting in reduced glucose consumption capacity and consequentially establishing the high-glucose microenvironment that fostered transcription of the T cell costimulatory molecule Cd27 via mTOR-FOXM1 signaling in infiltrating CD8+ T cells. Together, these data reveal that IFN-a reprograms glucose metabolism within HCC tumor microenvironment, thereby liberating T cell cytotoxic capacities and potentiating the PD-1 blockade-induced immune response. Our findings suggest that IFN-a and anti-PD-1 cotreatment is an effective novel combination strategy for HCC patients.

In patients with HCC and PVTT, PA-TACE was associated with a lower risk of death, particularly, among those with PVTT involving right/left or main portal vein, after excluding patients who were unsuitable for this procedure at 1 month after surgery.

Electrochemically active bacteria can transport their metabolically generated electrons to anodes, or accept electrons from cathodes to synthesize high‐value chemicals and fuels, via a process known as extracellular electron transfer (EET). Harnessing of this microbial EET process has led to the development of microbial bio‐electrochemical systems (BESs), which can achieve the interconversion of electrical and chemical energy and enable electricity generation, hydrogen production, electrosynthesis, wastewater treatment, desalination, water and soil remediation, and sensing. Here, the focus is on the current understanding of the microbial EET process occurring at both the bacteria–electrode interface and the biotic interface, as well as some attempts to improve the EET by using various nanomaterials. The behavior of nanomaterials in different EET routes and their influence on the performance of BESs are described. The inherent mechanisms will guide rational design of EET‐related materials and lead to a better understanding of EET mechanisms.

This study provides detailed information about survival outcomes and prognostic factors. Child-Pugh B value, uncontrolled intrahepatic tumor, LN location far from liver, and no response to EBRT are the unfavorable independent predictors.