Dynamic Bubbling Balanced Proactive CO2 Capture and Reduction on a Triple-Phase Interface Nanoporous Electrocatalyst.

The formation and preservation of the active phase of the catalysts at the triple-phase interface during CO2 capture and reduction is essential for improving the conversion efficiency of CO2 electroreduction toward value-added chemicals and fuels under operational conditions. Designing such ideal catalysts that can mitigate parasitic hydrogen generation and prevent active phase degradation during the CO2 reduction reaction (CO2RR), however, remains a significant challenge. Herein, we developed an interfacial engineering strategy to build a new SnOx catalyst by invoking multiscale approaches. This catalyst features a hierarchically nanoporous structure coated with an organic F-monolayer that modifies the triple-phase interface in aqueous electrolytes, substantially reducing competing hydrogen generation (less than 5%) and enhancing CO2RR selectivity (∼90%). This rationally designed triple-phase interface overcomes the issue of limited CO2 solubility in aqueous electrolytes via proactive CO2 capture and reduction. Concurrently, we utilized pulsed square-wave potentials to dynamically recover the active phase for the CO2RR to regulate the production of C1 products such as formate and carbon monoxide (CO). This protocol ensures profoundly enhanced CO2RR selectivity (∼90%) compared with constant potential (∼70%) applied at -0.8 V (V vs RHE). We further achieved a mechanistic understanding of the CO2 capture and reduction processes under pulsed square-wave potentials via in situ Raman spectroscopy, thereby observing the potential-dependent intensity of Raman vibrational modes of the active phase and CO2RR intermediates. This work will inspire material design strategies by leveraging triple-phase interface engineering for emerging electrochemical processes, as technology moves toward electrification and decarbonization.

M6A-mediated upregulation of lncRNA TUG1 in liver cancer cells regulates the antitumor response of CD8+ T cells and phagocytosis of macrophages.

Tumor immune evasion relies on the crosstalk between tumor cells and adaptive/innate immune cells. Immune checkpoints play critical roles in the crosstalk, and immune checkpoint inhibitors have achieved promising clinical effects. The long non-coding RNA taurine-upregulated gene 1 (TUG1) is upregulated in hepatocellular carcinoma (HCC). However, how TUG1 is upregulated and the effects on tumor immune evasion are incompletely understood. Here, METTL3-mediated m6A modification led to TUG1 upregulation is demonstrated. Knockdown of TUG1 inhibited tumor growth and metastasis, increased the infiltration of CD8+ T cells and M1-like macrophages in tumors, promoted the activation of CD8+ T cells through PD-L1, and improved the phagocytosis of macrophages through CD47. Mechanistically, TUG1 regulated PD-L1 and CD47 expressions by acting as a sponge of miR-141 and miR-340, respectively. Meanwhile, TUG1 interacted with YBX1 to facilitate the upregulation of PD-L1 and CD47 transcriptionally, which ultimately regulated tumor immune evasion. Clinically, TUG1 positively correlated with PD-L1 and CD47 in HCC tissues. Moreover, the combination of Tug1-siRNA therapy with a Pdl1 antibody effectively suppressed tumor growth. Therefore, the mechanism of TUG1 in regulating tumor immune evasion is revealed and can inform existing strategies targeting TUG1 for enhancing HCC immune therapy and drug development.

HDAC Inhibition Sensitize Hepatocellular Carcinoma to Lenvatinib via Suppressing AKT Activation.

Hepatocellular carcinoma (HCC) is a deadly malignancy with limited treatment options. As a first-line treatment for advanced HCC, Lenvatinib has been applicated in clinic since 2018. Resistance to Lenvatinib, however, has severely restricted the clinical benefits of this drug. Therefore, it is urgent to explore the potential resistance mechanisms of Lenvatinib and identify appropriate methods to reduce resistance for the treatment of HCC. We identified SAHA, a HDAC inhibitor, to have effective anti-tumor activity against Lenvatinib-resistant HCC organoids by screening a customized drug library. Mechanism analysis revealed that SAHA upregulates PTEN expression and suppresses AKT signaling, which contributes to reversing Lenvatinib resistance in liver cancer cells. Furthermore, combinational application of Lenvatinib and HDAC inhibitor or AKT inhibitor synergistically inhibits HCC cell proliferation and induces cell apoptosis. Finally, we confirmed the synergistic effects of Lenvatinib and SAHA, or AZD5363 in primary liver cancer patient derived organoids. Collectively, these findings may enable the development of Lenvatinib combination therapies for HCC.

Histamine-related genes participate in the establishment of an immunosuppressive microenvironment and impact the immunotherapy response in hepatocellular carcinoma.

Chronic inflammation is pivotal in the pathogenesis of hepatocellular carcinoma (HCC). Histamine is a biologically active substance that amplifies the inflammatory and immune response and serves as a neurotransmitter. However, knowledge of histamine's role in HCC and its effects on immunotherapy remains lacking. We focused on histamine-related genes to investigate their potential role in HCC. The RNA-seq data and clinical information regarding HCC were obtained from The Cancer Genome Atlas (TCGA). After identifying the differentially expressed genes, we constructed a signature using the univariate Cox proportional hazard regression and least absolute shrinkage and selection operator (LASSO) analyses. The signature's predictive performance was evaluated using a receiver operating characteristic curve (ROC) analysis. Furthermore, drug sensitivity, immunotherapy effects, and enrichment analyses were conducted. Histamine-related gene expression in HCC was confirmed using quantitative real-time polymerase chain reaction (qRT-PCR). A histamine-related gene prognostic signature (HRGPS) was developed in TCGA. Time-dependent ROC and Kaplan-Meier survival analyses demonstrated the signature's strong predictive power. Importantly, patients in high-risk groups exhibited a higher frequency of TP53 mutations, elevated immune checkpoint-related gene expression, and increased infiltration of immunosuppressive cells-indicating a potentially favorable response to immunotherapy. In addition, drug sensitivity analysis revealed that the signature could effectively predict chemotherapy efficacy and sensitivity. qRT-PCR results validated histamine-related gene overexpression in HCC. Our findings demonstrate that inhibiting histamine-related genes and signaling pathways can impact the therapeutic effect of anti-PD-1/PD-L1. The precise predictive ability of our signature in determining the response to different therapeutic options highlights its potential clinical significance.

RASSF4 Attenuates Metabolic Dysfunction-Associated Steatotic Liver Disease Progression via Hippo Signaling and Suppresses Hepatocarcinogenesis.

BACKGROUND & AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a dynamic chronic liver disease closely related to metabolic abnormalities such as diabetes and obesity. MASLD can further progress to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and even hepatocellular carcinoma (HCC). However, the mechanisms underlying the progression of MASLD and further progression to liver fibrosis and liver cancer are unknown. METHODS: In this study, we performed transcriptome analysis in livers from mice with MASLD and found suppression of a potential anti-oncogene, RAS association domain protein 4 (RASSF4). RASSF4 expression levels were measured in liver or tumor tissues of patients with MASH or HCC, respectively. We established RASSF4 overexpression and knockout mouse models. The effects of RASSF4 were evaluated by quantitative polymerase chain reaction, Western blotting, histopathological analysis, wound healing assays, Transwell assays, EdU incorporation assays, colony formation assays, sorafenib sensitivity assays, and tumorigenesis assays. RESULTS: RASSF4 was significantly down-regulated in MASH and HCC samples. Using liver-specific RASSF4 knockout mice, we demonstrated that loss of hepatic RASSF4 exacerbated hepatic steatosis and fibrosis. In contrast, RASSF4 overexpression prevented steatosis in MASLD mice. In addition, RASSF4 in hepatocytes suppressed the activation of hepatic stellate cells (HSCs) by reducing transforming growth factor beta secretion. Moreover, we found that RASSF4 is an independent prognostic factor for HCC. Mechanistically, we found that RASSF4 in the liver interacts with MST1 to inhibit YAP nuclear translocation through the Hippo pathway. CONCLUSIONS: These findings establish RASSF4 as a therapeutic target for MASLD and HCC.

Xinyang tablet alleviated cardiac dysfunction in a cardiac pressure overload model by regulating the receptor-interacting serum/three-protein kinase 3/FUN14 domain containing 1-mediated mitochondrial unfolded protein response and mitophagy.

ETHNOPHARMACOLOGICAL RELEVANCE: Xinyang tablet (XYT) has been used for heart failure (HF) for over twenty years in clinical practice, but the underlying molecular mechanism remains poorly understood. AIMS OF THE STUDY: In the present study, we aimed to explore the protective effects of XYT in HF in vivo and in vitro. MATERIALS AND METHODS: Transverse aortic constriction was performed in vivo to establish a mouse model of cardiac pressure overload. Echocardiography, tissue staining, and real-time quantitative PCR (qPCR) were examined to evaluate the protective effects of XYT on cardiac function and structure. Adenosine 5'-triphosphate production, reactive oxygen species staining, and measurement of malondialdehyde and superoxide dismutase was used to detect mitochondrial damage. Mitochondrial ultrastructure was observed by transmission electron microscope. Immunofluorescence staining, qPCR, and Western blotting were performed to evaluate the effect of XYT on the mitochondrial unfolded protein response and mitophagy, and to identify its potential pharmacological mechanism. In vitro, HL-1 cells and neonatal mouse cardiomyocytes were stimulated with Angiotensin II to establish the cell model. Western blotting, qPCR, immunofluorescence staining, and flow cytometry were utilized to determine the effects of XYT on cardiomyocytes. HL-1 cells overexpressing receptor-interacting serum/three-protein kinase 3 (RIPK3) were generated by transfection of RIPK3-overexpressing lentiviral vectors. Cells were then co-treated with XYT to determine the molecular mechanisms. RESULTS: In the present study, XYT was found to exerta protective effect on cardiac function and structure in the pressure overload mice. And it was also found XYT reduced mitochondrial damage by enhancing mitochondrial unfolded protein response and restoring mitophagy. Further studies showed that XYT achieved its cardioprotective role through regulating the RIPK3/FUN14 domain containing 1 (FUNDC1) signaling. Moreover, the overexpression of RIPK3 successfully reversed the XYT-induced protective effects and significantly attenuated the positive effects on the mitochondrial unfolded protein response and mitophagy. CONCLUSIONS: Our findings indicated that XYT prevented pressure overload-induced HF through regulating the RIPK3/FUNDC1-mediated mitochondrial unfolded protein response and mitophagy. The information gained from this study provides a potential strategy for attenuating mitochondrial damage in the context of pressure overload-induced heart failure using XYT.

Pharmacogenomic profiling of intra-tumor heterogeneity using a large organoid biobank of liver cancer.

Inter- and intra-tumor heterogeneity is a major hurdle in primary liver cancer (PLC) precision therapy. Here, we establish a PLC biobank, consisting of 399 tumor organoids derived from 144 patients, which recapitulates histopathology and genomic landscape of parental tumors, and is reliable for drug sensitivity screening, as evidenced by both in vivo models and patient response. Integrative analysis dissects PLC heterogeneity, regarding genomic/transcriptomic characteristics and sensitivity to seven clinically relevant drugs, as well as clinical associations. Pharmacogenomic analysis identifies and validates multi-gene expression signatures predicting drug response for better patient stratification. Furthermore, we reveal c-Jun as a major mediator of lenvatinib resistance through JNK and ß-catenin signaling. A compound (PKUF-01) comprising moieties of lenvatinib and veratramine (c-Jun inhibitor) is synthesized and screened, exhibiting a marked synergistic effect. Together, our study characterizes the landscape of PLC heterogeneity, develops predictive biomarker panels, and identifies a lenvatinib-resistant mechanism for combination therapy.

Clinical Outcomes at 3 Years After Stenting for Thrombotic and Non-thrombotic Iliac Vein Compression Syndrome Patients.

Iliac vein stenting for the treatment of iliac vein compression syndrome (IVCS) has been gradually developed. This article investigated the long-term patency and improvement of clinical symptoms after endovascular stenting for iliac vein obstruction patients. From 2020 to 2022, 83 patients at a single institution with IVCS underwent venous stent implantation and were divided into two groups: non-thrombotic IVCS (n = 55) and thrombotic IVCS (n = 28). The main stent-related outcomes include technical success, long-term patency, and thrombotic events. The technical success rate of all stent implantation was 100%. The mean length of hospital stay and cost were higher in the thrombotic IVCS group than in the non-thrombotic ICVS group, as well as the length of diseased vessel segment and the number of stents implanted were higher than in the control non-thrombotic group. The 1-, 2-, and 3-year patency rates were 85.4%, 80% and 66.7% in the thrombosis group, which were lower than 93.6%, 88.7%, and 87.5% in the control group (P = .0135, hazard ratio = 2.644). In addition, patients in both groups had a foreign body sensation after stent implantation, which resolved spontaneously within 1 year after surgery. Overall, there were statistically significant differences in long-term patency rate outcome between patients with thrombotic and non-thrombotic IVCS, the 1-, 2-, and 3-year patency rates in non-thrombotic IVCS patients were higher than those in thrombotic IVCS patients.

LINC00869 Promotes Hepatocellular Carcinoma Metastasis via Protrusion Formation.

Coordination of filament assembly and membrane remodeling is required for the directional migration of cancer cells. The Wiskott-Aldrich syndrome protein (WASP) recruits the actin-related protein (ARP) 2/3 complex to assemble branched actin networks. The goal of our study was to assess the potential regulatory role exerted by the novel long noncoding RNA (lncRNA) LINC00869 on hepatocellular carcinoma (HCC) cells. We used HCC cells to overexpress or knockdown LINC00869, analyzed patient data from publicly available databases and Cancer Hospital Affiliated with Zhengzhou University, and used a xenograft mouse model of HCC to study the molecular mechanism associated with LINC00869 expression. We found that high levels of LINC00869 expression were associated with poor prognosis in patients with HCC. Next, we detected an interaction between LINC00869 and both WASP and ARP2 in HCC cells, and observed a modulatory effect of LINC00869 on the phosphorylation of WASP at Y291 and the activity of cell division control protein 42 (CDC42). These modulatory roles were required for WASP/CDC42 activity on F-actin polymerization to enhance membrane protrusion formation and maintain persistent cell polarization. This, in turn, promoted the migration and invasion abilities of HCC cells. Finally, we confirmed the role of LINC00869in vivo, using the tumor xenograft mouse model; and identified a positive correlation between LINC00869 expression levels and the phosphorylation levels of WASP in HCC samples. Overall, our findings suggest a unique mechanism by which LINC00869 orchestrates membrane protrusion during migration and invasion of HCC cells. IMPLICATIONS: LncRNA LINC00869 regulates the activity of CDC42-WASP pathway and positively affects protrusion formation in HCC cells, which expands the current understanding of lncRNA functions as well as gives a better understanding of carcinogenesis.

Corrigendum: Unveiling the key genes, environmental toxins, and drug exposures in modulating the severity of ulcerative colitis: a comprehensive analysis.

[This corrects the article DOI: 10.3389/fimmu.2023.1162458.].

Reactive high-spin iron(IV)-oxo sites through dioxygen activation in a metal-organic framework.

In nature, nonheme iron enzymes use dioxygen to generate high-spin iron(IV)=O species for a variety of oxygenation reactions. Although synthetic chemists have long sought to mimic this reactivity, the enzyme-like activation of O2 to form high-spin iron(IV) = O species remains an unrealized goal. Here, we report a metal-organic framework featuring iron(II) sites with a local structure similar to that in α-ketoglutarate-dependent dioxygenases. The framework reacts with O2 at low temperatures to form high-spin iron(IV) = O species that are characterized using in situ diffuse reflectance infrared Fourier transform, in situ and variable-field Mössbauer, Fe Kß x-ray emission, and nuclear resonance vibrational spectroscopies. In the presence of O2, the framework is competent for catalytic oxygenation of cyclohexane and the stoichiometric conversion of ethane to ethanol.

Unveiling the key genes, environmental toxins, and drug exposures in modulating the severity of ulcerative colitis: a comprehensive analysis.

Background: As yet, the genetic abnormalities involved in the exacerbation of Ulcerative colitis (UC) have not been adequately explored based on bioinformatic methods. Materials and methods: The gene microarray data and clinical information were downloaded from Gene Expression Omnibus (GEO) repository. The scale-free gene co-expression networks were constructed by R package "WGCNA". Gene enrichment analysis was performed via Metascape database. Differential expression analysis was performed using "Limma" R package. The "randomForest" packages in R was used to construct the random forest model. Unsupervised clustering analysis performed by "ConsensusClusterPlus"R package was utilized to identify different subtypes of UC patients. Heat map was established using the R package "pheatmap". Diagnostic parameter capability was evaluated by ROC curve. The"XSum"packages in R was used to screen out small-molecule drugs for the exacerbation of UC based on cMap database. Molecular docking was performed with Schrodinger molecular docking software. Results: Via WGCNA, a total 77 high Mayo score-associated genes specific in UC were identified. Subsequently, the 9 gene signatures of the exacerbation of UC was screened out by random forest algorithm and Limma analysis, including BGN,CHST15,CYYR1,GPR137B,GPR4,ITGA5,LILRB1,SLFN11 and ST3GAL2. The ROC curve suggested good predictive performance of the signatures for exacerbation of UC in both the training set and the validation set. We generated a novel genotyping scheme based on the 9 signatures. The percentage of patients achieved remission after 4 weeks intravenous corticosteroids (CS-IV) treatment was higher in cluster C1 than that in cluster C2 (54% vs. 27%, Chi-square test, p=0.02). Energy metabolism-associated signaling pathways were significantly up-regulated in cluster C1, including the oxidative phosphorylation, pentose and glucuronate interconversions and citrate cycle TCA cycle pathways. The cluster C2 had a significant higher level of CD4+ T cells. The"XSum"algorithm revealed that Exisulind has a therapeutic potential for UC. Exisulind showed a good binding affinity for GPR4, ST3GAL2 and LILRB1 protein with the docking glide scores of -7.400 kcal/mol, -7.191 kcal/mol and -6.721 kcal/mol, respectively.We also provided a comprehensive review of the environmental toxins and drug exposures that potentially impact the progression of UC. Conclusion: Using WGCNA and random forest algorithm, we identified 9 gene signatures of the exacerbation of UC. A novel genotyping scheme was constructed to predict the severity of UC and screen UC patients suitable for CS-IV treatment. Subsequently, we identified a small molecule drug (Exisulind) with potential therapeutic effects for UC. Thus, our study provided new ideas and materials for the personalized clinical treatment plans for patients with UC.

Baicalin induces ferroptosis in osteosarcomas through a novel Nrf2/xCT/GPX4 regulatory axis.

BACKGROUND: Osteosarcomas (OS) is a kind of malignant bone tumor which occurs primarily in children and adolescents, and the clinical therapeutics remain disappointing. As a new programmed cell death, ferroptosis is characterized by iron dependent and intracellular oxidative accumulation, which provides a potential alternative intervene for the OS treatment. Baicalin, a major bioactive flavone derived from traditional Chinese medicine Scutellaria baicalensis, has been proved to have anti-tumor properties in OS. Whether ferroptosis participated in the baicalin mediated anti-OS activity is an interesting project. PURPOSE: To explore the pro-ferroptosis effect and mechanisms of baicalin in OS. METHODS/STUDY DESIGN: Pro-ferroptosis effect of baicalin on cell death, cell proliferation, iron accumulation, lipid peroxidation production was determined in MG63 and 143B cells. The levels of glutathione (GSH), oxidized (GSSG) glutathione and malondialdehyde (MDA) were determined by enzyme linked immunosorbent assay (ELISA). The expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), Glutathione peroxidase 4 (GPX4) and xCT were detected by western blot in baicalin-mediated ferroptosis regulation. In vivo, a xenograft mice model was adopted to explore the anticancer effect of baicalin. RESULTS: In the present study, it was found that baicalin significantly suppress tumor cell growth in vitro and in vivo. By promoting the Fe accumulation, ROS formation, MDA production and suppressing the ratio of GSH/GSSG, baicalin was found to trigger ferroptosis in OS and ferroptosis inhibitor ferrostatin-1 (Fer-1) successfully reversed these suppressive effects, indicating that ferroptosis participated in the baicalin mediated anti-OS activity. Mechanistically, baicalin physically interacted with Nrf2, a critical regulator of ferroptosis, and influenced its stability via inducing ubiquitin degradation, which suppressed the Nrf2 downstream targets GPX4 and xCT expression, and led to stimulating ferroptosis. CONCLUSIONS: Our findings for the first time indicated that baicalin exerted anti-OS activity through a novel Nrf2/xCT/GPX4-dependent ferroptosis regulatory axis, which hopefully provides a promising candidate for OS treatment.

Nitric oxide releasing polyvinyl alcohol and sodium alginate hydrogels as antibacterial and conductive strain sensors.

Conductive hydrogels have promising applications in flexible electronic devices and artificial intelligence, which have attracted much attention in recent years. However, most conductive hydrogels have no antimicrobial activity, inevitably leading to microbial infections during utilization. In this work, a series of antibacterial and conductive polyvinyl alcohol and sodium alginate (PVA-SA) hydrogels were successfully developed with the incorporation of S-nitroso-N-acetyl-penicillamine (SNAP) and MXene through a freeze-thaw approach. Due to the reversibility of hydrogen bonding and electrostatic interactions, the resulting hydrogels had excellent mechanical properties. Specifically, the presence of MXene readily interrupted the crosslinked hydrogel network, but the best stretching can reach up to >300 %. Moreover, the impregnation of SNAP achieved the release of nitric oxide (NO) over several days under physiological conditions. Due to the release of NO, these composited hydrogels demonstrated high antibacterial activities (> 99 %) against both Gram-positive and negative S. aureus and E. coli bacteria. Notably, the excellent conductivity of MXene endowed the hydrogel with a sensitive, fast, and stable strain-sensing ability, to accurately monitor and distinguish subtle physiological activities of the human body including finger bending and pulse beating. These novel composited hydrogels are likely to have potential as strain-sensing materials in the field of biomedical flexible electronics.

Hypsochromically-shifted Emission of Metal-organic Frameworks Generated through Post-synthetic Ligand Reduction.

Luminescent materials with tunable emission are becoming increasingly desirable as we move towards needing efficient Light Emitting Diodes (LEDs) for displays. Key to developing better displays is the advancement of strategies for rationally designing emissive materials that are tunable and efficient. We report a series of emissive metal-organic frameworks (MOFs) generated using BUT-10 (BUT: Beijing University of Technology) that emits green light with λmax at 525 nm. Post-synthetic reduction of the ketone on the fluorenone ligand in BUT-10 generates new materials, BUT-10-M and BUT-10-R. The emission for BUT-10-R is hypsochromically-shifted by 113 nm. Multivariate BUT-10-M structures demonstrate emission with two maxima corresponding to the emission of both fluorenol and fluorenone moieties present in their structures. Our study represents a novel post-synthetic ligand reduction strategy for producing emissive MOFs with tunable emission ranging from green, white-blue to deep blue.

In Situ Raman Study of Voltage Tolerance Up to 2.2 V of Ionic Liquid Analogue Supercapacitor Electrolytes Immune to Water Adsorption Conferred by Amphoteric Imidazole Additives.

Ionic liquid analogues (ILAs) are promising electrolytes for supercapacitors due to their low cost and considerable voltage (>2.0 V). However, the voltage is <1.1 V for water-adsorbed ILAs. Herein for the first time, an amphoteric imidazole (IMZ) additive is reported to address this concern by reconfiguring the solvent shell of ILAs. Addition of only 2 wt % IMZ increases the voltage from 1.1 to 2.2 V, with an increase in capacitance from 178 to 211 F g-1 and an increase in energy density from 6.8 to 32.6 Wh kg-1. In situ Raman reveals that the strong H-bonds formed by IMZ with completive ligands 1,3-propanediol and water induce a reversal of the polarity of the solvent shells, suppressing absorbed water electrochemical activity and thus increasing the voltage. This study solves the problem of low voltage for water-adsorbed ILAs and reduces the equipment cost of ILA-based supercapacitor assembly (e.g., assembly in air without a glovebox).

Enhanced Thermoelectric Performance of CoSb3 Thin Films by Ag and Ti Co-Doping.

The Skutterudites CoSb3 material has been the focus of research for the conversion applications of waste heat to electricity due to its ability to accommodate a large variety of ions in the cages that have been proven effective in improving the thermoelectric performance. Although the co-doped CoSb3 bulk materials have attracted increasing attention and have been widely studied, co-doped CoSb3 thin films have been rarely reported. In this work, Ag and Ti were co-doped into CoSb3 thin films via a facile in situ growth method, and the influence of doping content in the thermoelectric properties was investigated. The results show that all the Ag and Ti co-doped CoSb3 thin films contain a pure well-crystallized CoSb3 phase. Compared to the un-doped thin film, the co-doped samples show simultaneous increase in the Seebeck coefficient and the electrical conductivity, leading to a distinctly enhanced power factor. The high power factor value can reach ~0.31 mWm-1K-2 at 623 K after appropriate co-doping, which is two times the value of the un-doped thin film we have been obtained. All the results show that the co-doping is efficient in optimizing the performance of the CoSb3 thin films; the key point is to control the doping element content so as to obtain high thermoelectric properties.

LINC02870 facilitates SNAIL translation to promote hepatocellular carcinoma progression.

Exploring the roles of long noncoding RNAs (lncRNAs) in tumorigenesis and metastasis could contribute to the recognition of novel diagnostic and therapeutic targets. LINC02870 is a novel lncRNA, whose role in tumors has not been reported. Herein, we focused on the function and mechanism of LINC02870 in human hepatocellular carcinoma (HCC). We first carried out a pan-cancer study of LINC02870 expression and its relationship to prognosis, and LINC02870 was determined to be a possible oncogene in HCC. Upregulated expressions of LINC02870 were also found in our HCC samples compared to the para-tumor samples. Moreover, overexpression of LINC02870 promoted the growth, migration, and invasion of HCC cells. Subsequently, binding proteins of LINC02870 were identified by a number of in silico analyses, including correlation analysis, signaling network analysis, and survival analysis. Intriguingly, the most promising binding protein of LINC02870 was predicted and confirmed to be eukaryotic translation initiation factor 4 gamma 1 (EIF4G1), an important component of the eukaryotic translation initiation factor 4F complex that initiates cap-dependent translation. Further investigation showed that LINC02870 increased the translation of SNAIL to induce malignant phenotypes in HCC cells. Additionally, HCC patients with higher expression levels of LINC02870 and EIF4G1 had shorter survival times than those with lower expression levels. Thus, our findings suggested that LINC02870 induced SNAIL translation and correlated with poor prognosis and tumor progression in HCC.

Nitric oxide releasing alginate microspheres for antimicrobial application.

The controlled release of nitric oxide (NO) is significantly crucial in the NO-related biomedical field. In the current work, the controlled release of NO from alginate microspheres was achieved through the direct impregnation of S-nitroso-N-acetyl-penicillamine (SNAP) in the gelation of sodium alginate with calcium ions. The loading rate of SNAP in alginate microspheres was obtained in a range of 0.69 %­27.5 %. Specifically, the longest NO release time reached up to ∼93 h. Furthermore, the structure, thermal properties, and morphology were fully characterized. During the antibacterial studies, the NO-releasing spheres can produce a great bactericidal effect on Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). The alginate microspheres impregnated with 315 mg SNAP (sphere size: 2.88 mm) can effectively reduce the number of bacteria by 7 orders of magnitude with an inhibition rate up to 100 %. Therefore, we anticipated that these NO-releasing alginate microspheres would have great potential for biomedical-related applications.