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As global warming has become a major environmental problem, how to effectively reduce or rationally utilize greenhouse gases has become an important topic. This review summarizes the latest development of Ni-based catalysts for thermal-catalytic conversion of CO2 and CH4, including steam reforming of methane, partial oxidation of methane, methane decomposition, dry reforming of methane, reverse water gas shift reaction and CO2 hydrogenation. The modification strategies are illustrated in depth, such as size and dispersion control, surface modification, oxygen defects. Besides, the reaction and coking mechanisms for various processes are introduced, and the effects of reaction conditions and reactor designs are discussed and illustrated. This is the first comprehensive review on discussing the latest developments of anti-coking Ni-based catalysts for six commonly studied thermal-catalytic processes where two greenhouse gases (CH4 and CO2) are involved. To further improve the catalytic performances and energy efficiency, advanced techniques such as plasma and microwave can be integrated and in-situ characterizations are expected to explore the deactivation mechanisms in depth. Moreover, a smart design of the catalyst is necessary to inhibit the side reactions by changing the reaction pathways.

Time-delayed reservoir computing (RC) is a brain inspired paradigm for processing temporal information, with simplification in the network’s architecture using virtual nodes embedded in a temporal delay line. In this work, a novel, to the best of our knowledge, RC system based on a dual-loop optoelectronic oscillator is proposed to enhance the prediction and classification. The hardware is compact and easy to implement, and only a section of fiber compared to the traditional optoelectronic oscillator reservoir is added to conform the dual-loop scheme. Compared with the traditional reservoir, a remarkable performance of the proposed RC system is demonstrated by simulation on three well-known tasks, namely the nonlinear auto regressive moving average (NARMA10) task, signal waveform recognized task, and handwritten numeral recognition. The parameter optimization in the NARMA10 task is presented with influenced factors. The novel RC system finally obtains a normalized mean square error at 0.0493 ± 0.007 in NARMA10 task, 6.172 × 1 0 − 6 in signal waveform recognized task, and a word error rate at 9% in handwritten numeral recognition with suitable parameters.

An approach for simultaneous modulation format identification (MFI) and optical signal-to-noise ratio (OSNR) monitoring in digital coherent optical communications is proposed based on optoelectronic reservoir computing (RC) and the signal’s amplitude histograms (AHs) obtained after the adaptive post-equalization. The optoelectronic RC is implemented using a Mach-Zehnder modulator and optoelectronic delay feedback loop. We investigate the performance of the proposed model with the number of symbols, bins of AHs and the hyperparameters of optoelectronic RC. The results show that 100% MFI accuracy can be achieved simultaneously with accurate OSNR estimation for different modulation formats under study. The lowest achievable OSNR estimation mean absolute errors for the dual-polarization (DP)-quadrature phase-shift keying signal, the DP-16-ary quadrature amplitude modulation (16QAM) signal, and the DP-64QAM signal are 0.2 dB, 0.32 dB and 0.53 dB, respectively. The robustness of the proposed scheme is also evaluated when the optoelectronic RC is in presence of additive white Gaussian noises. Then, a proof of concept experiment is demonstrated to further verify our proposed method. The proposed approach offers a potential solution for next-generation intelligent optical performance monitoring in the physical layer.

Objectives Evidences demonstrate that sorafenib alleviates liver fibrosis via inhibiting HSC activation and ECM accumulation. The underlying mechanism remains unclear. Ferroptosis, a novel programmed cell death, regulates diverse physiological/pathological processes. In this study, we aim to investigate the functional role of HSC ferroptosis in the anti‐fibrotic effect of sorafenib. Materials and Methods The effects of sorafenib on HSC ferroptosis and ECM expression were assessed in mouse model of liver fibrosis induced by CCl4. In vitro, Fer‐1 and DFO were used to block ferroptosis and then explored the anti‐fibrotic effect of sorafenib by detecting α‐SMA, COL1α1 and fibronectin proteins. Finally, HIF‐1α siRNA, plasmid and stabilizers were applied to assess related signalling pathway. Results Sorafenib attenuated liver injury and ECM accumulation in CCl4‐induced fibrotic livers, accompanied by reduction of SLC7A11 and GPX4 proteins. In sorafenib‐treated HSC‐T6 cells, ferroptotic events (depletion of SLC7A11, GPX4 and GSH; accumulation iron, ROS and MDA) were discovered. Intriguingly, these ferroptotic events were not appeared in hepatocytes or macrophages. Sorafenib‐elicited HSC ferroptosis and ECM reduction were abrogated by Fer‐1 and DFO. Additionally, both HIF‐1α and SLC7A11 proteins were reduced in sorafenib‐treated HSC‐T6 cells. SLC7A11 was positively regulated by HIF‐1α, inactivation of HIF‐1α/SLC7A11 pathway was required for sorafenib‐induced HSC ferroptosis, and elevation of HIF‐1α could inhibit ferroptosis, ultimately limited the anti‐fibrotic effect. Conclusions Sorafenib triggers HSC ferroptosis via HIF‐1α/SLC7A11 signalling, which in turn attenuates liver injury and fibrosis., Sorafenib triggers hepatic stellate cell ferroptosis by inhibiting the HIF‐1α/SLC7A11 pathway to attenuate liver fibrosis. Treatment with sorafenib induces a decrease of HIF‐1α, which in turn reduces SLC7A11 expression in HSCs. Then leads to GPX4, GSH depletion and ROS excess, and ultimately induces HSC ferroptosis and ECM reduction.

Macrophages, diversity and plasticity immune cells, participate in immune response and maintain homeostasis through M1/M2 phenotype transformation. Transient receptor potential melastatin 7 (TRPM7) is a widely expressed divalent cation channel with protein serine/threonine kinase activity, which has recently been found to affect macrophage proliferation and function. This study aimed to identify the role of TRPM7 in macrophage polarization. Our results suggested that TRPM7 was highly expressed in M1-type macrophages rather than M2-type macrophages. Interestingly, we detected that M1-type macrophages decreased while M2-type macrophages enhanced through blockade of TRPM7, which manifest as decreased TNF-α, iNOS and elevated Arg-1, CD206. Furthermore, blockade of TRPM7 could inhibit STAT1 phosphorylation and promote STAT6 phosphorylation. In conclusion, TRPM7 could regulate macrophage polarization via STAT1/STAT6 pathways. Taken together, it is suggested that TRPM7 might serve as a molecular regulator in macrophage polarization and is a potential therapeutic target for inflammatory diseases.

Background Programmed cell death receptor 1 (PD-1) is an immunosuppressive molecule expressed on T cells, and its ligand (PD-L1) which expressed on tumor cells play pivotal roles in regulating host immune responses. However, little is known whether PD-1/PD-L1 axis could directly activates intracellular oncogenic signaling pathways in tumor cells, leading to tumor resistance. Methods In the present study, the expression of PD-1 and PD-L1 in the tissues of gastric cancer was detected by western blot and immunofluorescence. The effect of PD-L1-Fc and cisplatin on resistant gastric cancer cells was examined by MTT assay and Flow Cytometry. In addition. The effect of PD-L1-Fc on the expression of P-gp in gastric cancer cells and resistant gastric cancer cells was detected by quantitative real-time reverse-transcription PCR (qRT-PCR) and western blot. The molecular mechanisms of the regulation of cisplatin and PD-L1-Fc treatment were evaluated by western blot. Results We found that the level of PD-1 was significantly increased in human gastric cancer tissues and drug-resistant gastric cancer cells and P-gp was the same result. The PD-L1 could reduce the level of cell damage caused by cisplatin. In addition, we found PD-L1 can also up-regulate the expression of P-gp. Mechanistically, PD-L1 activated the PI3K/AKT signaling pathway in which PI3K/AKT pathway inhibition attenuated the upregulation of P-gp. Conclusion PD-1/PD-L1 enhanced cisplatin resistance in gastric cancer through PI3K/AKT mediated P-gp expression.

In this study, we report a self-template hydrothermal method for the synthesis of ATiO3 (A = Ba, Pb, and Sr) perovskites using anatase TiO2 nanosheets as precursors. Under hydrothermal conditions, ATiO3 with different structures and morphology can be obtained. These samples were characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM) and transmission electron microscopy (TEM) techniques. The growth mechanism of ATiO3 was explored by XRD evaluation over different reaction time, and it was observed that PbTiO3 grows most slowly among all the samples including BaTiO3, SrTiO3, BaxPb1−xTiO3 and SrxPb1−xTiO3. The diffusion of A site sources to the solid surface and the reaction at solid/liquid interface could dominate the growth of ATiO3. All the as-prepared samples exhibited activities toward photocatalytic oxidation of NO at ppb level. Specifically, PbTiO3 has revealed the highest activity under both full spectrum and visible-light irradiation (λ > 420 nm), whereas BaTiO3 exhibited best selectivity for the formation of ionic species (NO3−), which could be ascribed to different electronic structures and charge separation efficiency of ATiO3. This study provides some important hints to tune the photocatalytic performances (activity and selectivity) of ATiO3 through the modification of A site elements.

Liver fibrosis is a compensatory response to the tissue repair process. The activation and proliferation of hepatic stellate cells (HSCs) are thought to be related to the occurrence of hepatic fibrosis. Therefore, inhibiting the activation and proliferation of HSCs is a key step in alleviating liver fibrosis. As a non-specific inhibitor of transient receptor potential melastatin 7 (TRPM7), carvacrol has anti-tumor, anti-inflammatory and anti-hepatic fibrosis activities. This study aimed to explore the protective effect of carvacrol on liver fibrosis and related molecular mechanisms. A CCl4-induced liver fibrosis mouse model and platelet-derived growth factor (PDGF-BB)-activated HSC-T6 cells (a rat hepatic stellate cell line) were employed for in vivo and in vitro experiments. C57BL/6J mice were orally administered different concentrations of carvacrol every day for 6 weeks during the development of CCl4-induced liver fibrosis. The results show that carvacrol could effectively reduce liver damage and the progression of liver fibrosis in mice, which are expressed as fibrotic markers levels were reduced and histopathological characteristics were improved. Moreover, carvacrol inhibited the proliferation and activation of HSC-T6 cells induced by PDGF-BB. In addition, it was found that carvacrol inhibits the expression of TRPM7 and mediated through mitogen-activated protein kinases (MAPK). Collectively, our study shows that carvacrol can reduce liver fibrosis by inhibiting the activation and proliferation of hepatic stellate cells, and the MAPK signaling pathway might be involved in this process.

Strontium titanate (SrTiO3) nanocrystals have been synthesized by a hydrothermal reaction route using anatase TiO2 nanosheets with dominant {001} facets and commercial anatase TiO2 nanoparticles as precursors. Time-resolved quenching experiments showed that the speed of hydrothermal formation of SrTiO3 was relatively fast (in minutes). The initial particle morphology and exposed crystal facets of anatase TiO2 precursor cannot be retained in the final SrTiO3 products. SrTiO3 nuclei are formed by the reaction between Ti(OH)x4−x and Sr ions at the TiO2 solid/liquid interface. As surface adsorbed F− is necessary to stabilize the {001} facets of anatase TiO2, the hydrothermal crystallization of SrTiO3 from TiO2 with {001} facets not only exhibits a slower reaction rate but also a higher activation energy. Moreover, the photoelectrochemical and photocatalytic activity studies indicated that the SrTiO3 products obtained from TiO2 with {001} facets showed enhanced photocurrent density and photocatalytic hydrogen production activity. The present study sheds some light on the understanding of the crystal facets of the precursor on the hydrothermal formation process as well as the photocatalytic activities of the corresponding products.

Hydrogen evolution through photocatalysis is promising with respect to the environmental problems and challenges of energy shortage that we encounter today. In this paper, we have combined graphene quantum dots (GQDs) and {001} faceted anatase TiO2 (with an exposed percentage of 65–75%) together for effective photocatalytic hydrogen evolution. A series of characterizations including X-ray diffraction, transmission electron microscopy, X-ray photoelectron spectroscopy, Fourier-transform infrared spectroscopy and UV-visible absorption spectroscopy have been carried out to study the structure of the as-prepared GQDs/{001}TiO2 composite. It turns out that GQDs could be effectively decorated on {001}TiO2 sheet without changing its intrinsic structure. With an optimum loading amount of GQDs (0.5 wt% to {001}TiO2), GQDs/{001}TiO2 exhibits a hydrogen evolution efficiency 8 times higher than that of bare {001}TiO2, which is a significantly more obvious improvement than many other photocatalytic systems relevant to GQDs and TiO2 hybrids. In addition, GQDs/{001}TiO2 could stand long-term photocatalytic experiments. Photocurrent tests show that such an improvement of the photocatalytic efficiency over GQDs/{001}TiO2 may originate from a higher charge separation efficiency. The present study could offer reference for the construction of photocatalytic hydrogen evolution systems with low cost and long term stability.