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To address the alignment difficulties in precision assembly, this paper designs an adaptive position correction system. The system integrates electromagnetic proportional control technology to optimize the alignment mechanism, making its floating range linearly adjustable. This solution overcomes the issue of incompatible alignment mechanisms for workpieces of different sizes, providing a new approach to solving position deviation problems in precision assembly.

This paper summarized the main detection methods of paraquat, including the instrumental analysis like HPLC, GC, LC-MS/MS, and so on. The re- search prospects of paraquat detection were also put forward.

The long non-coding RNA PVT1 (lncRNA PVT1) has been reported to act as an oncogenic regulator of several cancers. However, its expression and function in gallbladder cancer (GBC) remain largely unknown. In situ hybridization (ISH) and quantitative real-time PCR (qPCR) were performed to detect the expression of PVT1 and miR-143 in GBC tissues and cell lines. Immunohistochemistry (IHC) assays were performed to assess the expression of the hexokinase 2 (HK2) protein. The relationships among PVT1, miR-143 and HK2 were evaluated using dual-luciferase reporter, RNA immunoprecipitation (RIP) and biotin pull-down assays. The biological functions of PVT1, miR-143 and HK2 in GBC cells were explored with cell counting kit 8 (CCK-8), 5-ethynyl-20-deoxyuridine (EdU), colony formation, transwell, wound healing and glucose metabolism assays in vitro. For in vivo experiments, a xenograft model was used to investigate the effects of PVT1 and HK2 on GBC. PVT1 was upregulated in GBC tissues and cells and was positively associated with malignancies and worse overall survival. PVT1 knockdown inhibited cell proliferation, migration, and invasion in vitro and restrained tumor growth in vivo. Further studies demonstrated that PVT1 positively regulated HK2 expression via its competing endogenous RNA (ceRNA) activity on miR-143. Additionally, HK2 expression and function were positively correlated with PVT1. Furthermore, we observed that the PVT1/miR-143/HK2 axis promoted cell proliferation and metastasis by regulating aerobic glucose metabolism in GBC cells. The results of our study reveal a potential ceRNA regulatory pathway in which PVT1 modulates HK2 expression by competitively binding to endogenous miR-143 in GBC cells, which may provide new insights into novel molecular therapeutic targets for GBC.

Our previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.

Recently, with the foundation and development of gene ontology (GO) resources, numerous works have been proposed to compute functional similarity of genes and achieved series of successes in some research fields. Focusing on the calculation of the information content (IC) of terms is the main idea of these methods, which is essential for measuring functional similarity of genes. However, most approaches have some deficiencies, especially when measuring the IC of both GO terms and their corresponding annotated term sets. To this end, measuring functional similarity of genes accurately is still challenging. In this article, we proposed a novel gene functional similarity calculation method, which especially encapsulates the specificity of terms and edges (STE). The proposed method mainly contains three steps. Firstly, a novel computing model is put forward to compute the IC of terms. This model has the ability to exploit the specific structural information of GO terms. Secondly, the IC of term sets are computed by capturing the genetic structure between the terms contained in the set. Lastly, we measure the gene functional similarity according to the IC overlap ratio of the corresponding annotated genes sets. The proposed method accurately measures the IC of not only GO terms but also the annotated term sets by leveraging the specificity of edges in the GO graph. We conduct experiments on gene functional classification in biological pathways, gene expression datasets, and protein-protein interaction datasets. Extensive experimental results show the better performances of our proposed STE against several baseline methods.

This study aims to investigate the influence of clay mineral content on the rheological properties and long-term deformation stability of clays, and to establish a unified model capable of quantitatively describing the nonlinear rheological behavior of clays with different mineral compositions. Direct shear rheological tests were conducted on specimens prepared with different mixing ratios of bentonite, kaolin, and quartz. Combined with micro-mechanism analysis, the controlling factors of clay rheological behavior were explored. The experimental results show that the creep stress threshold, elastic viscosity, and average plastic viscosity decrease significantly with increasing clay mineral content. The rheological deformation exhibits distinct nonlinear characteristics, and clay mineral content plays a controlling role in the rheological behavior. Based on experimental and mechanistic analysis, a unified rheological model was established, which reflects the material origin of rheology and captures nonlinear rheological characteristics. This model can predict the entire time-history mechanical behavior of clays with different mineral compositions across the three stages of instantaneous deformation, decay rheology, and steady-state rheology under different shear stress levels using a single set of parameters. Validation was performed through direct shear rheological tests under 50 working conditions for five types of clay specimens, demonstrating good consistency between the model calculations and experimental results. The unified rheological model reveals the material origin and physical essence of clay rheology, demonstrates high universality, and advances the understanding of the influence of mineral composition on rheology from the current phenomenological qualitative description to quantitative calculation for the first time, significantly enhancing its engineering application value. This provides a more reliable tool for predicting long-term deformation and assessing the stability of clay foundations.

CD8 + T cell exhaustion dampens antitumor immunity. Although several transcription factors have been identified that regulate T cell exhaustion, the molecular mechanisms by which CD8 + T cells are triggered to enter an exhausted state remain unclear. Here, we show that interleukin-2 (IL-2) acts as an environmental cue to induce CD8 + T cell exhaustion within tumor microenvironments. We find that a continuously high level of IL-2 leads to the persistent activation of STAT5 in CD8 + T cells, which in turn induces strong expression of tryptophan hydroxylase 1, thus catalyzing the conversion to tryptophan to 5-hydroxytryptophan (5-HTP). 5-HTP subsequently activates AhR nuclear translocation, causing a coordinated upregulation of inhibitory receptors and downregulation of cytokine and effector-molecule production, thereby rendering T cells dysfunctional in the tumor microenvironment. This molecular pathway is not only present in mouse tumor models but is also observed in people with cancer, identifying IL-2 as a novel inducer of T cell exhaustion. IL-2 is a classic T cell growth factor. Huang and colleagues demonstrate, however, that chronic IL-2 stimulation leads to a new exhaustion pathway that impairs antitumor immune responses.

In search of effective and stable bifunctional electrocatalyst for electrocatalytic water splitting is still a major challenge for the highly efficient H 2 production. Here, we reported a facile strategy to design high-indexed Cu 3 Pd 13 S 7 nanoparticles (NPs) in situ synthesized on the three-dimensional (3D) carbon nanofibers (CNFs) by combining electrospinning and chemical vapor deposition (CVD) technology. The high-index facets with abundant active sites, the 3D architecture CNFs with high specific surface area and synergistic effect of Cu–Pd–S bonds with strong electron couplings together promote the electrocatalytic performance. The Cu 3 Pd 13 S 7 /CNFs shows excellent electrocatalytic activity with low overpotentials of 52 mV (10 mA cm −2 ) for hydrogen evolution reaction (HER) and 240 mV (10 mA cm −2 ) for oxygen evolution reaction (OER). The excellent protection of Cu 3 Pd 13 S 7 by CNFs from aggregation and electrolyte corrosion lead to the high stability of Cu 3 Pd 13 S 7 /CNFs under acidic and alkaline conditions.

Limiting fuel sulfur content (FSC) is a widely adopted approach for reducing ship emissions of sulfur dioxide (SO2) and particulate matter (PM), particularly in emission control areas (ECAs), but its impact on the emissions of volatile organic compounds (VOCs) is still not well understood. In this study, emissions from ships at berth in Guangzhou, southern China, were characterized before and after the implementation of the fuel switch policy (IFSP) with an FSC limit of 0.5 % in the Pearl River Delta ECA (ECA-PRD). After IFSP, the emission factors (EFs) of SO2 and PM2.5 for the coastal vessels decreased by 78 % and 56 % on average, respectively; however, the EFs of the VOCs were 1807±1746 mg kg−1, approximately 15 times that of 118±56.1 mg kg−1 before IFSP. This dramatic increase in the emissions of the VOCs might have been largely due to the replacement of high-sulfur residual fuel oil with low-sulfur diesel or heavy oils, which are typically richer in short-chain hydrocarbons. Moreover, reactive alkenes surpassed alkanes to become the dominant group among the VOCs, and low-carbon-number VOCs, such as ethylene, propene and isobutane, became the dominant species after IFSP. As a result of the largely elevated EFs of the reactive alkenes and aromatics after IFSP, the emitted VOCs per kilogram of fuel burned had nearly 29 times greater ozone formation potential (OFP) and approximately 2 times greater secondary organic aerosol formation potential (SOAFP) than those before IFSP. Unlike the coastal vessels, the river vessels in the region used diesel fuels consistently and were not affected by the fuel switch policy, but the EFs of their VOCs were 90 % greater than those of the coastal vessels after IFSP, with approximately 120 % greater fuel-based OFP and 70 %–140 % greater SOAFP. The results from this study suggest that while the fuel switch policy could effectively reduce SO2 and PM emissions, and thus help control PM2.5 pollution, it will also lead to greater emissions of reactive VOCs, which may threaten ozone pollution control in harbor cities. This change for coastal or ocean-going vessels, in addition to the large amounts of reactive VOCs from the river vessels, raises regulatory concerns for ship emissions of reactive VOCs.

Mechanical force contributes to perforin pore formation at immune synapses, thus facilitating the cytotoxic T lymphocytes (CTL)-mediated killing of tumor cells in a unidirectional fashion. How such mechanical cues affect CTL evasion of perforin-mediated autolysis remains unclear. Here we show that activated CTLs use their softness to evade perforin-mediated autolysis, which, however, is shared by T leukemic cells to evade CTL killing. Downregulation of filamin A is identified to induce softness via ZAP70-mediated YAP Y357 phosphorylation and activation. Despite the requirements of YAP in both cell types for softness induction, CTLs are more resistant to YAP inhibitors than malignant T cells, potentially due to the higher expression of the drug-resistant transporter, MDR1, in CTLs. As a result, moderate inhibition of YAP stiffens malignant T cells but spares CTLs, thus allowing CTLs to cytolyze malignant cells without autolysis. Our findings thus hint a mechanical force-based immunotherapeutic strategy against T cell leukemia. Cell softness protects cytotoxic T lymphocytes (CTL) from autolysis by own soluble factors such as perforin secreted for killing target cells. Here the authors show that softness can be induced by YAP activation, and that T leukemic cells are more sensitive to YAP inhibition than CTLs, thereby hinting YAP inhibitors as a potential therapy for T leukemia.