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Abstract For the multistage progression of prostate cancer (PCa) and resistance to immunotherapy, tumour‐associated macrophage is an essential contributor. Although immunotherapy is an important and promising treatment modality for cancer, most patients with PCa are not responsive towards it. In addition to exploring new therapeutic targets, it is imperative to identify highly immunotherapy‐sensitive individuals. This research aimed to establish a signature risk model, which derived from the macrophage, to assess immunotherapeutic responses and predict prognosis. Data from the UCSC‐XENA, GEO and TISCH databases were extracted for analysis. Based on both single‐cell datasets and bulk transcriptome profiles, a macrophage‐related score (MRS) consisting of the 10‐gene panel was constructed using the gene set variation analysis. MRS was highly correlated with hypoxia, angiogenesis, and epithelial‐mesenchymal transition, suggesting its potential as a risk indicator. Moreover, poor immunotherapy responses and worse prognostic performance were observed in the high‐MRS group of various immunotherapy cohorts. Additionally, APOE, one of the constituent genes of the MRS, affected the polarisation of macrophages. In particular, the reduced level of M2 macrophage and tumour progression suppression were observed in PCa xenografts which implanted in Apolipoprotein E‐knockout mice. The constructed MRS has the potential as a robust prognostic prediction tool, and can aid in the treatment selection of PCa, especially immunotherapy options.

Study region: The study area comprises 336 administrative units located in mainland China. Study focus: The research aims at better understanding the relationship between regional industrial water use efficiency (IWUE) and the economic development level (EDL) that drives its annual variation, and to create a conceptual model to simulate these variations. A method is proposed for estimating regional IWUE for the following year via parameter calibration and extension in mainland China. New hydrological insights for the region: A conceptual model is developed to simulate annual regional IWUE(water use per 10,000 yuan of industrial added value) variation driven by EDL(GDP per capita). The model has an even number of hyperbola lines indicating log-transformed IWUE state fluctuations relative to EDL index. The model is derived based on three key findings. The categorical hyperbolic correlation between the EDL and IWUE allows similar model structure in different rank match levels. Second, multi-year data sets can calibrate the shape parameter because the hyperbola's shape remains constant over the years. Furthermore, regional IWUE can be predicted by the hyperbola's linear location with year. The model offers a new quantitative analysis method for setting regional IWUE control red lines in China. It could also serve as a foundation for studying the relationship between IWUE and other socio-economic characteristics in different nations and developing regional and possibly worldwide IWUE model construction and parameterization.

Abstract Using user-generated content (UGC) is of utmost importance for e-commerce platforms to extract valuable commercial information. In this paper, we propose an explainable multimodal learning approach named the visual–semantic embedding model with a self-attention mechanism for multimodal interaction (VSEM-SAMMI) to predict user-generated image (UGI) helpfulness and product sales. Focusing on SHEIN (i.e. a fast-fashion retailer), we collect the images posted by consumers, along with product and portrait characteristics. Moreover, we use VSEM-SAMMI, which adopts a self-attention mechanism to enforce attention weights between image and text, to extract features from UGI then use machine learning algorithms to predict UGI helpfulness and product sales. We explain features using a caption generation model and test the predictive power of embeddings and portrait characteristics. The results indicate that when predicting commercial information, embeddings are more informative than product and portrait characteristics. Combining VSEM-SAMMI with light gradient boosting (LightGBM) yields a mean squared error (MSE) of 0.208 for UGI helpfulness prediction and 0.184 for product sales prediction. Our study offers valuable insights for e-commerce platforms, enhances feature extraction from UGI through image–text joint embeddings for UGI helpfulness and product sales prediction, and pioneers a caption generation model for interpreting image embeddings in the e-commerce domain.

Elevated brain angiotensin II activity plays a key role in the development of neurogenic hypertension. While blood pressure (BP) control in neurogenic hypertension has been successfully demonstrated by regulating central angiotensin II activity, current techniques involving cerebrovascular injections of potential therapeutic agents are not suitable for clinical translation. To address this gap, we present the synthesis of dual-functionalized liposomes functionalized with targeting ligand and cell-penetrating peptide. Functionalized liposomes were synthesized using the thin film hydration technique and loaded with plasmid DNA encoding short hairpin RNA targeted toward angiotensin II receptors (PEAS), via the post-insertion method. The synthesized liposomes had a cationic surface charge, an average size of 150 nm, and effectively entrapped more than 89% of loaded PEAS. These liposomes loaded with PEAS demonstrated biocompatibility and efficient delivery to brain-derived cell lines, resulting in a remarkable reduction of more than 70% in receptor expression within 7 days. To assess the therapeutic potential, spontaneously hypertensive rats were administered intravenous injections of functionalized liposomes loaded with PEAS, and the changes in mean arterial pressure were monitored for 45 days. Remarkably, this treatment led to a significant (p

Lignocellulosic materials, made up of cellulose, hemicellulose, and lignin, constitute some of the most prevalent types of biopolymers in marine ecosystems. The degree to which marine microorganisms participate in the breakdown of lignin and their impact on the cycling of carbon in the oceans is not well understood. Strain LCG002, a novel Marivivens species isolated from Lu Chao Harbor’s intertidal seawater, is distinguished by its ability to metabolize lignin and various aromatic compounds, including benzoate, 3-hydroxybenzoate, 4-hydroxybenzoate and phenylacetate. It also demonstrates a broad range of carbon source utilization, including carbohydrates, amino acids and carboxylates. Furthermore, it can oxidize inorganic gases, such as hydrogen and carbon monoxide, providing alternative energy sources in diverse marine environments. Its diversity of nitrogen metabolism is supported by nitrate/nitrite, urea, ammonium, putrescine transporters, as well as assimilatory nitrate reductase. For sulfur assimilation, it employs various pathways to utilize organic and inorganic substrates, including the SOX system and DSMP utilization. Overall, LCG002’s metabolic versatility and genetic profile contribute to its ecological significance in marine environments, particularly in the degradation of lignocellulosic material and aromatic monomers.

Abstract Background The American Joint Committee on Cancer (AJCC) 8th staging system of prostate cancer may be insufficient in predicting the prognosis of some staged patients. This study aimed to modify the AJCC 8th staging system in patients with advanced prostate cancer. Methods Data of patients with advanced prostate cancer from the Surveillance, Epidemiology, and End Results (SEER) database between 2004 and 2016 were enrolled in this cohort study. All patients were divided into the training set and the testing set with a ratio of 6:4. Multivariate Cox survival model was utilized to obtain the nomogram score for each stage variable. The modified staging system was based on the total nomogram score. The C-index and Kaplan-Meier (K-M) curves were used to show the prognostic prediction effect of patients with different staging systems. Results A total of 28,006 patients were included for analysis. T stage, N stage, M stage, primary Gleason pattern score, secondary Gleason pattern score, and PSA level were included as stage variables. Patients with AJCC stage III C [hazard ratio (HR) = 4.17, 95% confidence interval (CI), 3.39–5.13] and AJCC stage IV B (HR = 3.19, 95%CI, 1.79–5.69) were associated with worse prognosis compared with those of AJCC stage III B, while no statistical significance was found in patients with stage IV A (P > 0.05). In terms of the modified staging system, patients with modified stage III C (HR = 2.06, 95%CI, 1.46–2.92), modified stage IV A (HR = 6.91, 95%CI, 4.81–9.94), and modified stage IV B (HR = 21.89, 95%CI, 14.76–32.46) were associated with a poorer prognosis compared with patients with modified stage III B. The prognostic ability (C-index) of the modified staging system (0.789; 95%CI, 0.777–0.801) was better than that of the AJCC 8th edition system (0.762; 95%CI, 0.748–0.776) (0.789 vs. 0.762, P = 0.004). The K-M curves indicated that the modified staging system may be distinguished prognostic differences in patients with different stages. Conclusion Modified staging system may be better than AJCC 8th staging system for predicting prognosis in prostate cancer patients. The AJCC 8th staging system should be further optimized.

Lignocellulosic materials are composed of cellulose, hemicellulose and lignin and are one of the most abundant biopolymers in marine environments. The extent of the involvement of marine microorganisms in lignin degradation and their contribution to the oceanic carbon cycle remains elusive. In this study, a novel lignin-degrading bacterial strain, LCG003, was isolated from intertidal seawater in Lu Chao Harbor, East China Sea. Phylogenetically, strain LCG003 was affiliated with the genus Aliiglaciecola within the family Alteromonadaceae. Metabolically, strain LCG003 contains various extracellular (signal-fused) glycoside hydrolase genes and carbohydrate transporter genes and can grow with various carbohydrates as the sole carbon source, including glucose, fructose, sucrose, rhamnose, maltose, stachyose and cellulose. Moreover, strain LCG003 contains many genes of amino acid and oligopeptide transporters and extracellular peptidases and can grow with peptone as the sole carbon and nitrogen source, indicating a proteolytic lifestyle. Notably, strain LCG003 contains a gene of dyp-type peroxidase and strain-specific genes involved in the degradation of 4-hydroxy-benzoate and vanillate. We further confirmed that it can decolorize aniline blue and grow with lignin as the sole carbon source. Our results indicate that the Aliiglaciecola species can depolymerize and mineralize lignocellulosic materials and potentially play an important role in the marine carbon cycle.

Mechanisms by which BKCa (large-conductance calcium-sensitive potassium) channels are involved in vascular remodeling in hypertension are not fully understood. Vascular smooth muscle cell (VSMC) proliferation and vascular morphology were compared between hypertensive and normotensive rats. BKCa channel activity, protein expression, and interaction with IP3R (inositol 1,4,5-trisphosphate receptor) were examined using patch clamp, Western blot analysis, and coimmunoprecipitation. On inside-out patches of VSMCs, the Ca2+-sensitivity and voltage-dependence of BKCa channels were similar between hypertensive and normotensive rats. In whole-cell patch clamp configuration, treatment of cells with the IP3R agonist, Adenophostin A (AdA), significantly increased BKCa channel currents in VSMCs of both strains of rats, suggesting IP3R-BKCa coupling; however, the AdA-induced increases in BKCa currents were attenuated in VSMCs of hypertensive rats, indicating possible IP3R-BKCa decoupling, causing BKCa dysfunction. Co-immunoprecipitation and Western blot analysis demonstrated that BKCa and IP3R proteins were associated together in VSMCs; however, the association of BKCa and IP3R proteins was dramatically reduced in VSMCs of hypertensive rats. Genetic disruption of IP3R-BKCa coupling using junctophilin-2 shRNA dramatically augmented Ang II-induced proliferation in VSMCs of normotensive rats. Subcutaneous infusion of NS1619, a BKCa opener, to reverse BKCa dysfunction caused by IP3R-BKCa decoupling significantly attenuated vascular hypertrophy in hypertensive rats. In summary, the data from this study demonstrate that loss of IP3R-BKCa coupling in VSMCs induces BKCa channel dysfunction, enhances VSMC proliferation, and thus, may contribute to vascular hypertrophy in hypertension.

Apelin, by stimulation of APJ receptors, induces transient blood pressure (BP) reduction and positive inotropic effects. APJ receptors share high homology with the Ang II type 1 receptor; thus, apelin was proposed to play a protective role in cardiovascular disease by antagonizing the actions of Ang II. In this regard, apelin and apelin-mimetics are currently being studied in clinical trials. However, the chronic effect of apelin in cardiovascular regulation has not been fully investigated. In the current study, blood pressure (BP) and heart rate (HR) were recorded using a telemetry implantation approach in conscious rats, before and during chronic subcutaneous infusion of apelin-13, using osmotic minipumps. At the end of the recording, the cardiac myocyte morphology was examined using H&E staining, and cardiac fibrosis was evaluated by Sirius Red in each group of rats. The results demonstrated that the chronic infusion of apelin-13 did not change either BP or HR. However, under the same condition, the chronic infusion of Ang II induced significant BP elevation, cardiac hypertrophy, and fibrosis. Co-administration of apelin-13 did not significantly alter the Ang II-induced elevation in BP, changes in cardiac morphology, and fibrosis. Taken together, our experiments showed an unexpected result indicating that the chronic administration of apelin-13 did not alter basal BP, nor did it change Ang II-induced hypertension and cardiac hypertrophy. The findings suggest that an APJ receptor biased agonist could be a better therapeutic alternative for treatment of hypertension.

Shewanella species are widely distributed in various environments, especially deep-sea sediments, due to their remarkable ability to utilize multiple electron receptors and versatile metabolic capabilities. In this study, a novel facultatively anaerobic, psychrophilic, and piezotolerant bacterium, Shewanella sp. MTB7, was isolated from the Mariana Trench at a depth of 5900 m. Here, we report its complete genome sequence and adaptation strategies for survival in deep-sea environments. MTB7 contains what is currently the third-largest genome among all isolated Shewanella strains and shows higher coding density than neighboring strains. Metabolically, MTB7 is predicted to utilize various carbon and nitrogen sources. D-amino acid utilization and HGT-derived purine-degrading genes could contribute to its oligotrophic adaptation. For respiration, the cytochrome o ubiquinol oxidase genes cyoABCDE, typically expressed at high oxygen concentrations, are missing. Conversely, a series of anaerobic respiratory genes are employed, including fumarate reductase, polysulfide reductase, trimethylamine-N-oxide reductase, crotonobetaine reductase, and Mtr subunits. The glycine reductase genes and the triplication of dimethyl sulfoxide reductase genes absent in neighboring strains could also help MTB7 survive in low-oxygen environments. Many genes encoding cold-shock proteins, glycine betaine transporters and biosynthetic enzymes, and reactive oxygen species-scavenging proteins could contribute to its low-temperature adaptation. The genomic analysis of MTB7 will deepen our understanding of microbial adaptation strategies in deep-sea environments.

Abstract Background Sialic acids are widely distributed in animal tissues, and aberrantly expressed in a variety of cancer types. High expression of sialic acid contributes to tumor aggressiveness by promoting cell proliferation, migration, angiogenesis, and metastasis. Sialidases are responsible for removal of sialic acids from glycoproteins and glycolipids. Methods N-glycomics of bladder cancer cells were detected by MALDI-TOF mass spectrometry. Sialic acid modification in bladder cancer tissue was determined by lectin blot. The down-regulation of NEU1 in bladder cancer cells was determined by high resolution liquid chromatography mass spectrometry (HR LC-MS). The effects of sialidase NEU1 expression on proliferation and apoptosis of human bladder cancer cells were examined by western blot, RT-PCR, confocal imaging and flow cytometry. Moreover, the function of sialic acids on fibronectin-integrin α5β1 interaction were assayed by immunoprecipitation and ELISA. The importance of NEU1 in tumor formation in vivo was performed using BALB/c-nu mice. Expression of NEU1 in primary human bladder cancer tissue samples was estimated using bladder cancer tissue microarray. Results (1) Downregulation of NEU1 was primarily responsible for aberrant expression of sialic acids in bladder cancer cells. (2) Decreased NEU1 expression was correlated with bladder cancer progression. (3) NEU1 overexpression enhanced apoptosis and reduced proliferation of bladder cancer cells. (4) NEU1 disrupted FN-integrin α5β1 interaction and deactivated the Akt signaling pathway. (5) NEU1 significantly suppressed in vivo tumor formation in BALB/c-nu mice. Conclusions Our data showed that NEU1 inhibited cancer cell proliferation, induced apoptosis, and suppressed tumor formation both in vitro and in vivo, by disrupting interaction of FN and integrin β1 and inhibiting the Akt signaling pathway. Our observations indicate that NEU1 is an important modulator of the malignant properties of bladder cancer cells, and is a potential therapeutic target for prognosis and treatment of bladder cancer. Video Abstract Graphical abstract

Hypertension is a major health concern globally. Elevated blood pressure, initiated and maintained by the brain, is defined as neurogenic hypertension (NH), which accounts for nearly half of all hypertension cases. A significant increase in angiotensin II-mediated sympathetic nervous system activity within the brain is known to be the key driving force behind NH. Blood pressure control in NH has been demonstrated through intracerebrovascular injection of agents that reduce the sympathetic influence on cardiac functions. However, traditional antihypertensive agents lack effective brain permeation, making NH management extremely challenging. Therefore, developing strategies that allow brain-targeted delivery of antihypertensives at the therapeutic level is crucial. Targeting nanotherapeutics have become popular in delivering therapeutics to hard-to-reach regions of the body, including the brain. Despite the frequent use of nanotherapeutics in other pathological conditions such as cancer, their use in hypertension has received very little attention. This review discusses the underlying pathophysiology and current management strategies for NH, as well as the potential role of targeted therapeutics in improving current treatment strategies.

Apelin-APJ receptor signaling regulates vascular tone in cerebral and peripheral arteries. We recently reported that apelin inhibits BKCa channel function in cerebral arteries, resulting in impaired endothelium-dependent relaxations. In contrast, apelin causes endothelium-dependent relaxation of coronary arteries. However, the effects of apelin on BKCa channel function in coronary arterial myocytes have not yet been explored. We hypothesized that apelin-APJ receptor signaling does not have an inhibitory effect on coronary arterial BKCa channels and hence does not alter nitric oxide (NO)-dependent relaxation of coronary arteries. Patch clamp recording was used to measure whole cell K+ currents in freshly isolated coronary smooth muscle cells. Apelin had no effect on the increases in current density in response to membrane depolarization or to NS1619 (a BKCa channel opener). Moreover, apelin did not inhibit NO/cGMP-dependent relaxations that required activation of BKCa channels in isolated coronary arteries. Apelin-APJ receptor signaling caused a marked increase in intracellular Ca2+ levels in coronary arterial smooth muscle cells, but failed to activate PI3-kinase to increase phosphorylation of Akt protein. Collectively, these data provide mechanistic evidence that apelin has no inhibitory effects on BKCa channel function in coronary arteries. The lack of inhibitory effect on BKCa channels makes it unlikely that activation of APJ receptors in coronary arteries would adversely affect coronary flow by creating a vasoconstrictive environment. It can be expected that apelin or other APJ receptor agonists in development will not interfere with the vasodilator effects of endogenous BKCa channel openers.

Cardiac hypertrophy is an adaptive response to cardiac overload initially but turns into a decompensated condition chronically, leading to heart failure and sudden cardiac death. The molecular mechanisms involved in cardiac hypertrophy and the signaling pathways that contribute to the switch from compensation to decompensation are not fully clear. The aim of the current study was to examine the role of PI3-kinases Class I (PI3KC1) and Class III (PI3KC3) in angiotensin (Ang) II-induced cardiac hypertrophy. The results demonstrate that treatment of cardiomyocytes with Ang II caused dose-dependent increases in autophagy, with an increasing phase followed by a decreasing phase. Ang II-induced autophagic increases were potentiated by inhibition of PI3KC1 with LY294002, but were impaired by inhibition of PI3KC3 with 3-methyladenine (3-MA). In addition, blockade of PI3KC1 significantly attenuated Ang II-induced ROS production and cardiomyocyte hypertrophy. In contrast, blockade of PI3KC3 potentiated Ang II-induced ROS production and cardiac hypertrophy. Moreover, blockade of PI3KC1 by overexpression of dominant negative p85 subunit of PI3KC1 significantly attenuated Ang II-induced cardiac hypertrophy in normotensive rats. Taken together, these results demonstrate that both PI3KC1 and PI3KC3 are involved in Ang II-induced cardiac hypertrophy by different mechanisms. Activation of PI3KC1 impairs autophagy activity, leading to accumulation of mitochondrial ROS, and, hence, cardiac hypertrophy. In contrast, activation of PI3KC3 improves autophagy activity, thereby reducing mitochondrial ROS and leads to a protective effect on Ang II-induced cardiac hypertrophy.

In this study, three-dimensional numerical studies have been performed to investigate the performance of a rotating detonation combustor with a diverging nozzle downstream. The effects of a diverging nozzle on the formation and propagation process of a detonation wave and typical flow field parameters in a rotating detonation combustor are mainly discussed. The results indicate that the diverging nozzle downstream is an important factor affecting the performance and design of a rotating detonation combustor. The diverging nozzle does not affect the formation and propagation process of the rotating detonation wave, while the time of two key wave collisions are delayed during the formation process of the detonation wave. With increases of the diverging angle, the rotating detonation combustor with the diverging nozzle can still maintain a certain pressure gain performance. Both the diverging nozzle and diverging angle have great influence on the flow field parameters of the rotating detonation combustor, including reducing the high pressure and temperature load, making the distribution of the outlet parameters uniform, and changing the local supersonic flow at the outlet. Among them, the outlet static pressure is reduced by up to 88.32%, and the outlet static temperature is reduced by up to 32.12%. This evidently improves the working environment of the combustor while reducing the thermodynamic and aerodynamic loads at the outlet. In particular, the diverging nozzle does not affect the supersonic characteristics of the outlet airflow, and on this basis, the Mach number becomes coincident and enhanced.

Hypertension represents a major risk factor for cardiovascular events, associating with vascular hypertrophy and dysfunction in resistance vessels. Clevidipine is a novel antihypertensive drug working as a selective calcium channel antagonist with an ultra-short half-life that lowers arterial blood pressure by reducing systemic arterial resistance. The aim was to assess the effect of clevidipine on the hypertrophic vessels of profilin1 hypertensive transgenic mice compared to sodium nitroprusside (SNP) and labetalol using wire myograph techniques. The effects of clevidipine, SNP and labetalol on the hypertrophic vessels were studied on mesenteric arterial function from 8 profilin1 hypertrophic mice and eight non-transgenic controls. Our results showed a significant difference between the effects of the three drugs on the hypertrophic mesenteric arteries of transgenic profilin1 mice compared to the non-transgenic controls. The half maximal effective concentration (EC50) of clevidipine, SNP and labetalol in profilin1 mice (1.90 ± 0.05, 0.97 ± 0.07, 2.80 ± 0.05 nM, respectively) were significantly higher than the EC50 in non-transgenic controls (0.91 ± 0.06, 0.32 ± 0.06, 0.80 ± 0.09 nM, respectively). Moreover, the increase in the EC50 for clevidipine (2-fold) to produce the same effect on both normal and hypertrophic arteries was less than that of SNP (3-fold) and labetalol (3.5-fold). Therefore, we concluded clevidipine exhibited the lowest dose shift to relax the hypertrophic vessels compared to SNP and labetalol in the profilin1 hypertrophic animal mouse model.

The best way to increase patient survival rate is to identify patients who are likely to progress to muscle-invasive or metastatic disease upfront and treat them more aggressively. The human cell lines HCV29 (normal bladder epithelia), KK47 (low grade nonmuscle invasive bladder cancer, NMIBC), and YTS1 (metastatic bladder cancer) have been widely used in studies of molecular mechanisms and cell signaling during bladder cancer (BC) progression. However, little attention has been paid to global quantitative proteome analysis of these three cell lines. We labeled HCV29, KK47, and YTS1 cells by the SILAC method using three stable isotopes each of arginine and lysine. Labeled proteins were analyzed by 2D ultrahigh-resolution liquid chromatography LTQ Orbitrap mass spectrometry. Among 3721 unique identified and annotated proteins in KK47 and YTS1 cells, 36 were significantly upregulated and 74 were significantly downregulated with >95% confidence. Differential expression of these proteins was confirmed by western blotting, quantitative RT-PCR, and cell staining with specific antibodies. Gene ontology (GO) term and pathway analysis indicated that the differentially regulated proteins were involved in DNA replication and molecular transport, cell growth and proliferation, cellular movement, immune cell trafficking, and cell death and survival. These proteins and the advanced proteome techniques described here will be useful for further elucidation of molecular mechanisms in BC and other types of cancer.

Apelin-13 causes vasoconstriction by acting directly on APJ receptors in vascular smooth muscle (VSM) cells; however, the ionic mechanisms underlying this action at the cellular level remain unclear. Large-conductance Ca(2+)-activated K(+) (BKCa) channels in VSM cells are critical regulators of membrane potential and vascular tone. In the present study, we examined the effect of apelin-13 on BK(Ca) channel activity in VSM cells, freshly isolated from rat middle cerebral arteries. In whole-cell patch clamp mode, apelin-13 (0.001-1 μM) caused concentration-dependent inhibition of BK(Ca) in VSM cells. Apelin-13 (0.1 µM) significantly decreased BK(Ca) current density from 71.25 ± 8.14 pA/pF to 44.52 ± 7.10 pA/pF (n=14 cells, P

Epithelial-to-mesenchymal transition (EMT) is an essential biological process involved in embryonic development, cancer progression, and metastatic diseases. EMT has often been used as a model for elucidating the mechanisms that underlie bladder cancer progression. However, no study to date has addressed the quantitative global variation of proteins in EMT using normal and non-malignant bladder cells. We treated normal bladder epithelial HCV29 cells and low grade nonmuscle invasive bladder cancer KK47 cells with transforming growth factor-beta (TGF-β) to establish an EMT model, and studied non-treated and treated HCV29 and KK47 cells by the stable isotope labeling amino acids in cell culture (SILAC) method. Labeled proteins were analyzed by 2D ultrahigh-resolution liquid chromatography/LTQ Orbitrap mass spectrometry. Among a total of 2994 unique identified and annotated proteins in HCV29 and KK47 cells undergoing EMT, 48 and 56 proteins, respectively, were significantly upregulated, and 106 and 24 proteins were significantly downregulated. Gene ontology (GO) term analysis and pathways analysis indicated that the differentially regulated proteins were involved mainly in enhancement of DNA maintenance and inhibition of cell-cell adhesion. Proteomes were compared for bladder cell EMT vs. bladder cancer cells, revealing 16 proteins that displayed similar changes in the two situations. Studies are in progress to further characterize these 16 proteins and their biological functions in EMT.

Purpose: This paper aims to investigate the effect of Ti3SiC2 on the high-temperature tribological behaviors of NiCr coating, which was beneficial to improve the friction-wear performance of hot work mold. Design/methodology/approach: NiCr-Ti3SiC2 coatings were prepared on H13 steel substrate by laser cladding. The microstructure, phases and hardness of obtained coatings were analyzed using a super-depth of field microscope, X-ray diffraction and microhardness tester, respectively, and the tribological performance of obtained coatings at 500°C was investigated using a high-temperature tester. Findings: The results show the NiCr-Ti3SiC2 coatings are comprised of γ-Ni solid, solution, TixNiy, TiC and Ti3SiC2 phases, and the coating hardness is increased with the increase of Ti3SiC2 mass fraction, which is contributed to the fine-grain and dispersion strengthening effect by the addition of Ti3SiC2. The NiCr-Ti3SiC2 coatings present excellent friction reduction and wear resistance by the synergetic action of Ti3SiC2 lubricant and hard phase, and the wear mechanism is predominated by abrasive wear and oxidation wear. Originality/value: Ti3SiC2 phase was used to reinforce the tribological performance of H13 steel at high temperature, and the roles of friction reduction and wear resistance were discussed. Peer review: The peer review history for this article is available at: https://publons.com/publon/10.1108/ILT-01-2023-0004/ [ABSTRACT FROM AUTHOR]