We establish a powerful poly(4-styrenesulfonate) (PSS)-treated strategy for sulfur vacancy healing in monolayer MoS2 to precisely and steadily tune its electronic state. The self-healing mechanism, in which the sulfur vacancies are healed spontaneously by the sulfur adatom clusters on the MoS2 surface through a PSS-induced hydrogenation process, is proposed and demonstrated systematically. The electron concentration of the self-healed MoS2 dramatically decreased by 643 times, leading to a work function enhancement of ∼150 meV. This strategy is employed to fabricate a high performance lateral monolayer MoS2 homojunction which presents a perfect rectifying behaviour, excellent photoresponsivity of ∼308 mA W−1 and outstanding air-stability after two months. Unlike previous chemical doping, the lattice defect-induced local fields are eliminated during the process of the sulfur vacancy self-healing to largely improve the homojunction performance. Our findings demonstrate a promising and facile strategy in 2D material electronic state modulation for the development of next-generation electronics and optoelectronics.

BackgroundCD8+ T cells differentiate into exhausted status within tumors, including hepatocellular carcinoma (HCC), which constitutes a solid barrier to effective anti-tumor immunity. A detailed characterization of exhausted T cells and their prognostic value in HCC is lacking.MethodsWe collected fresh tumor tissues with adjacent non-tumor liver tissues and blood specimens of 56 HCC patients, as well as archived samples from two independent cohorts of HCC patients (n = 358 and n = 254), who underwent surgical resection. Flow cytometry and multiplex immunostaining were used to characterize CD8+ T cells. Patient prognosis was evaluated by Kaplan-Meier analysis and Cox regression analysis.ResultsCD8+ T cells were classified into three distinct subpopulations: PD1Hi, PD1Int and PD1−. PD1Hi CD8+ T cells were significantly enriched in tumor compared to adjacent non-tumor liver tissues. PD1Hi CD8+ T cells highly expressed exhaustion-related inhibitory receptors (TIM3, CTLA-4, etc.) and transcription factors (Eomes, BATF, etc.). In addition, PD1Hi CD8+ T cells expressed low levels of cytotoxic molecules and displayed a compromised capacity to produce pro-inflammatory cytokines while the expression of anti-inflammatory IL-10 was up-regulated following mitotic stimulation. Furthermore, PD1Hi CD8+ T cells shared features with tissue resident memory T cells and were also characterized in an aberrantly activated status with an apoptosis-prone potential. In two independent cohorts of HCC patients (n = 358 and n = 254), we demonstrated that PD1Hi or TIM3+PD1Hi CD8+ T cells were significantly correlated with poor prognosis, and the latter was positioned in close proximity to PD-L1+ tumor associated macrophages.ConclusionThe current study unveils the unique features of PD1Hi CD8+ exhausted T cells in HCC, and also suggests that exhausted T cells could act as a biomarker to select the most care-demanding patients for tailored therapies.

The dry reforming of methane was systematically studied over a series (2-30 wt%) of Co (~5nm in size) loaded CeO2 catalysts, with an effort to elucidate the behavior of Co and ceria in the catalytic process using in-situ methods. For the systems under study, the reaction activity scaled with increasing Co loading, and a 10 wt% Co-CeO2 catalyst exhibiting the best catalytic activity and good stability at 500 °C with little evidence for carbon accumulation. The phase transitions and the nature of active components in the catalyst were investigated during pretreatment and under reaction conditions by ex-situ/in-situ techniques including X-ray diffraction (XRD) and ambient-pressure X-ray photoelectron spectroscopy (AP-XPS). These studies showed a dynamical evolution in the chemical composition of the catalysts under reaction conditions. A clear transition of Co3O4 → CoO → Co, and Ce 4+ to Ce 3+ , was observed during the temperature programmed reduction under H2 and CH4. However, introduction of CO2, led to partial re-oxidation of all components at low temperatures, followed by reduction at high temperatures. Under optimum CO and H2 producing conditions both XRD and AP-XPS indicated that the active phase involved a majority of metallic Co with a small amount of CoO both supported on a partially reduced ceria (Ce 3+ /Ce 4+). We identified the importance of dispersing Co, anchoring it onto ceria surface sites, and then utilizing the redox properties of ceria for activating and then oxidatively converting methane while inhibiting coke formation. Furthermore, a synergistic effect between cobalt and ceria and the interfacial site are essential to successfully close the catalytic cycle.

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Excess iron has been reported to lead to osteoblastic cell damage, which is a crucial pathogenesis of iron overload-related osteoporosis. However, the cytotoxic mechanisms have not been fully documented. In the present study, we focused on whether necroptosis contributes to iron overload-induced osteoblastic cell death and related underlying mechanisms. Here, we showed that the cytotoxicity of iron overload in osteoblastic cells was mainly due to necrosis, as evidenced by the Hoechst 33258/PI staining, Annexin-V/PI staining, and transmission electronic microscopy. Furthermore, we revealed that iron overload-induced osteoblastic necrosis might be mediated via the RIPK1/RIPK3/MLKL necroptotic pathway. In addition, we also found that iron overload was able to trigger mitochondrial permeability transition pore (mPTP) opening, which is a critical downstream event in the execution of necroptosis. The key finding of our experiment was that iron overload-induced necroptotic cell death might depend on reactive oxygen species (ROS) generation, as N-acetylcysteine effectively rescued mPTP opening and necroptotic cell death. ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation. In summary, iron overload induced necroptosis of osteoblastic cells in vitro, which is mediated, at least in part, through the RIPK1/RIPK3/MLKL pathway. We also highlight the critical role of ROS in the regulation of iron overload-induced necroptosis in osteoblastic cells.