SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1.

Dysregulation of histone lysine methyltransferases and demethylases is one of the major mechanisms driving the epigenetic reprogramming of transcriptional networks in castration-resistant prostate cancer (CRPC). In addition to their canonical histone targets, some of these factors can modify critical transcription factors, further impacting oncogenic transcription programs. Our recent report demonstrated that LSD1 can demethylate the lysine 270 of FOXA1 in prostate cancer (PCa) cells, leading to the stabilization of FOXA1 chromatin binding. This process enhances the activities of the androgen receptor and other transcription factors that rely on FOXA1 as a pioneer factor. However, the identity of the methyltransferase responsible for FOXA1 methylation and negative regulation of the FOXA1-LSD1 oncogenic axis remains unknown. SETD7 was initially identified as a transcriptional activator through its methylation of histone 3 lysine 4, but its function as a methyltransferase on nonhistone substrates remains poorly understood, particularly in the context of PCa progression. In this study, we reveal that SETD7 primarily acts as a transcriptional repressor in CRPC cells by functioning as the major methyltransferase targeting FOXA1-K270. This methylation disrupts FOXA1-mediated transcription. Consistent with its molecular function, we found that SETD7 confers tumor suppressor activity in PCa cells. Moreover, loss of SETD7 expression is significantly associated with PCa progression and tumor aggressiveness. Overall, our study provides mechanistic insights into the tumor-suppressive and transcriptional repression activities of SETD7 in mediating PCa progression and therapy resistance.

LncRNA CHROMR/miR-27b-3p/MET axis promotes the proliferation, invasion, and contributes to rituximab resistance in diffuse large B-cell lymphoma.

Long non-coding RNAs (LncRNAs) could regulate chemoresistance through sponging microRNAs (miRNAs) and sequestering RNA binding proteins. However, the mechanism of lncRNAs in rituximab resistance in diffuse large B-cell lymphoma (DLBCL) is largely unknown. Here, we investigated the functions and molecular mechanisms of lncRNA CHROMR in DLBCL tumorigenesis and chemoresistance. LncRNA CHROMR is highly expressed in DLBCL tissues and cells. We examined the oncogenic functions of lncRNA CHROMR in DLBCL by a panel of gain-or-loss-of-function assays and in vitro experiments. LncRNA CHROMR suppression promotes CD20 transcription in DLBCL cells and inhibits rituximab resistance. RNA immunoprecipitation, RNA pull-down, and dual luciferase reporter assay reveal that lncRNA CHROMR sponges with miR-27b-3p to regulate mesenchymal-epithelial transition factor (MET) levels and Akt signaling in DLBCL cells. Targeting the lncRNA CHROMR/miR-27b-3p/MET axis reduces DLBCL tumorigenesis. Altogether, these findings provide a new regulatory model, lncRNA CHROMR/miR-27b-3p/MET, which can serve as a potential therapeutic target for DLBCL.

The causality between systemic inflammatory regulators and chronic respiratory diseases: A bidirectional Mendelian-randomization study.

INTRODUCTION: Accumulative evidence suggests the associations between systemic inflammatory regulators and chronic respiratory diseases (CRDs). However, the intrinsic causation remains implicit. Therefore, this study aimed to examine causative associations by mendelian randomization (MR) and to identify valuable active factors. METHODS: Based on data from the GWAS database, we performed MR analyses of 41 serum cytokines from 8,293 Finnish and European descent cohorts from GBMI and UKBB for five major CRDs. We mainly applied inverse variance weighted regression, supplemented by MR-Egger regression, weighted median, maximum likelihood, weighted mode, and simple mode algorithms. Moreover, sensitivity analyses were conducted using Cochrane's Q test, MR-Egger intercept, MR-PRESSO Global test and MR-Steiger filtering. Eventually, the consistency of MR results was assessed by leave-one-out. RESULTS: Our results suggest that 12 genetically predicted systemic inflammatory regulators probably participate in the progression of CRDs, including four risk factors (IL-1RA, IL-4, MIP-1A, PDGF-BB) and one protective factor (IL-6) in IPF, two protective factors (SCF, SDF-1A) in COPD, and two protective factors (SCF, SDF-1A) in asthma, two protective factors (GROA, IL-2RA) were also included in asthma, whereas only one factor (HGF) was protective against bronchiectasis. Additionally, two protective factors (FGF-BASIC, G-CSF) were identified in sarcoidosis. Sensitivity analyses showed no horizontal pleiotropy and significant heterogeneity. Finally, based on the findings of inverse MR analysis, no inverse causal association was uncovered, confirming the robustness of results. CONCLUSION: Our study unearths potential associations between systemic inflammatory modulators and common CRDs, providing new insights for inflammation-mediated CRD prevention and therapeutic approaches.

Cold atmospheric plasma for chronic kidney disease-related skin disorders.

BACKGROUND AND HYPOTHESIS: An estimated 80% of individuals with chronic kidney disease (CKD) experience concomitant skin disorders, yet experimental research that elucidates the pathological changes in CKD-affected skin is limited. Cold atmospheric plasma (CAP) has shown promise in regulating keratinocyte proliferation, skin barrier function, and anti-inflammatory activity. We hypothesize that CAP emerges as a promising therapeutic avenue for CKD-related skin diseases. METHODS: Male and female C57/BL6 mice were administered a 0.2% adenine diet to generate a CKD mouse model. Skin samples from dialysis patients were also collected. These models were used to investigate the pathological alterations in the renal glomeruli, tubules, and epidermis. Subsequently, the potential impact of CAP on the stratum corneum, keratinocytes, skin hydration, and inflammation in mice with CKD were examined. RESULTS: Renal biopsies revealed glomerular and tubular atrophy, epithelial degeneration and necrosis in uriniferous tubules, and significant renal interstitial fibrosis. Skin biopsies from patients with CKD and mice showed stratum corneum thickening, epidermis atrophy, skin hydration dysfunction, and excessive inflammation. CAP attenuated skin atrophy, hydration dysfunction, and inflammation in mice with CKD, as evidenced by the activated level of YAP1/ß-catenin and Nrf-2/OH-1, enhanced expression of K5 and Ki67, increased levels of AQP3, collagen I, and GLUT1, reduced infiltration of CD3+ T cells, and diminished levels of IL-6 and TNF-α. CONCLUSION: This study provides valuable insights into the pathological changes in skin associated with CKD in both patients and animal models. It also establishes that CAP has the potential to effectively mitigate skin atrophy, hydration dysfunction, and inflammation, suggesting a novel therapeutic avenue for the treatment of CKD-related skin disorders.

Integration of Hollow Microneedle Arrays with Jellyfish-Shaped Electrochemical Sensor for the Detection of Biomarkers in Interstitial Fluid.

This study integrates hollow microneedle arrays (HMNA) with a novel jellyfish-shaped electrochemical sensor for the detection of key biomarkers, including uric acid (UA), glucose, and pH, in artificial interstitial fluid. The jellyfish-shaped sensor displayed linear responses in detecting UA and glucose via differential pulse voltammetry (DPV) and chronoamperometry, respectively. Notably, the open circuit potential (OCP) of the system showed a linear variation with pH changes, validating its pH-sensing capability. The sensor system demonstrates exceptional electrochemical responsiveness within the physiological concentration ranges of these biomarkers in simulated epidermis sensing applications. The detection linear ranges of UA, glucose, and pH were 0~0.8 mM, 0~7 mM, and 4.0~8.0, respectively. These findings highlight the potential of the HMNA-integrated jellyfish-shaped sensors in real-world epidermal applications for comprehensive disease diagnosis and health monitoring.

TRIM29 acts as a potential senescence suppressor with epigenetic activation in nasopharyngeal carcinoma.

Epigenetic alterations marked by DNA methylation are frequent events during the early development of nasopharyngeal carcinoma (NPC). We identified that TRIM29 is hypomethylated and overexpressed in NPC cell lines and tissues. TRIM29 silencing not only limited the growth of NPC cells in vitro and in vivo, but also induced cellular senescence, along with reactive oxygen species (ROS) accumulation. Mechanistically, we found that TRIM29 interacted with voltage-dependent anion-selective channel 1 (VDAC1) to activate mitophagy clearing up damaged mitochondria, which are the major source of ROS. In patients with NPC, high levels of TRIM29 expression are associated with an advanced clinical stage. Moreover, we detected hypomethylation of TRIM29 in patient nasopharyngeal swab DNA. Our findings indicate that TRIM29 depends on VDAC1 to induce mitophagy and prevents cellular senescence by decreasing ROS. Detection of aberrantly methylated TRIM29 in the nasopharyngeal swab DNA could be a promising strategy for the early detection of NPC.

Rutaecarpine induces the differentiation of triple-negative breast cancer cells through inhibiting fumarate hydratase.

BACKGROUND: Triple-negative breast cancer (TNBC) is one of the most aggressive human cancers and has poor prognosis. Approximately 80% of TNBC cases belong to the molecular basal-like subtype, which can be exploited therapeutically by inducing differentiation. However, the strategies for inducing the differentiation of TNBC remain underexplored. METHODS: A three-dimensional (3D) morphological screening model based on a natural compound library was used to identify possible candidate compounds that can induce TNBC cell differentiation. The efficacy of rutaecarpine was verified using assays: RT-qPCR, RNA-seq, flow cytometry, immunofluorescence, SCENITH and label-free LC-MS/MS. The direct targets of rutaecarpine were identified through drug affinity responsive target stability (DARTS) assay. A xenograft mice model was also constructed to confirm the effect of rutaecarpine in vivo. RESULTS: We identified that rutaecarpine, an indolopyridoquinazolinone, induces luminal differentiation of basal TNBC cells in both 3D spheroids and in vivo mice models. Mechanistically, rutaecarpine treatment leads to global metabolic stress and elevated ROS in 3D cultured TNBC cells. Moreover, NAC, a scavenger of ROS, impedes rutaecarpine-induced differentiation of TNBC cells in 3D culture. Finally, we identified fumarate hydratase (FH) as the direct interacting target of rutaecarpine. The inhibition of FH and the knockdown of FH consistently induced the differentiation of TNBC cells in 3D culture. CONCLUSIONS: Our results provide a platform for differentiation therapy drug discovery using 3D culture models and identify rutaecarpine as a potential compound for TNBC treatment.

Dasatinib in combination with BMS-754807 induce synergistic cytotoxicity in lung cancer cells through inhibiting lung cancer cell growth, and inducing autophagy as well as cell cycle arrest at the G1 phase.

Lung cancer is the leading cause of cancer-related deaths worldwide. Combination of drugs targeting independent signaling pathways would effectively block the proliferation of cancer cells with lower concentrations and stronger synergy effects. Dasatinib, a multi-targeted protein tyrosine kinase inhibitor targeting BCR-ABL and kinases of SRC family, has been successfully applied in the treatment of chronic myeloid leukemia (CML). BMS-754807, an inhibitor targeting the insulin-like growth factor 1 receptor (IGF-IR) and insulin receptor (IR) family kinases, has been in phase I development for the treatment of a variety of human cancers. Herein, we demonstrated that dasatinib in combination with BMS-754807 inhibited lung cancer cell growth, while induced autophagy as well as cell cycle arrest at the G1 phase. Dasatinib in combination with BMS-754807 suppressed the expression of cell cycle marker proteins, Rb, p-Rb, CDK4, CDK6 and Cyclin D1, and the PI3K/Akt/mTOR signaling pathway. Dasatinib in combination with BMS-754807 induced autophagy in lung cancer cells, evidenced by the upregulation of LC3B II and beclin-1, the downregulation of LC3B I and SQSTM1/p62, and the autophagic flux observed with a confocal fluorescence microscopy. Furthermore, dasatinib (18 mg/kg) in combination with BMS-754807 (18 mg/kg) inhibited the growth of tumors in NCI-H3255 xenografts without changing the bodyweight. Overall, our results suggest that dasatinib in combination with BMS-754807 inhibits the lung cancer cell proliferation in vitro and tumor growth in vitro, which indicates promising evidence for the application of the drug combination in lung cancer therapy.

Exploiting the tumor-suppressive activity of the androgen receptor by CDK4/6 inhibition in castration-resistant prostate cancer.

The androgen receptor (AR) plays a pivotal role in driving prostate cancer (PCa) development. However, when stimulated by high levels of androgens, AR can also function as a tumor suppressor in PCa cells. While the high-dose testosterone (high-T) treatment is currently being tested in clinical trials of castration-resistant prostate cancer (CRPC), there is still a pressing need to fully understand the underlying mechanism and thus develop treatment strategies to exploit this tumor-suppressive activity of AR. In this study, we demonstrate that retinoblastoma (Rb) family proteins play a central role in maintaining the global chromatin binding and transcriptional repression program of AR and that Rb inactivation desensitizes CRPC to the high-dose testosterone treatment in vitro and in vivo. Using a series of patient-derived xenograft (PDX) CRPC models, we further show that the efficacy of high-T treatment can be fully exploited by a CDK4/6 inhibitor, which strengthens the chromatin binding of the Rb-E2F repressor complex by blocking the hyperphosphorylation of Rb proteins. Overall, our study provides strong mechanistic and preclinical evidence on further developing clinical trials to combine high-T with CDK4/6 inhibitors in treating CRPC.

Large-Scale Ultrafast Strain Engineering of CVD-Grown Two-Dimensional Materials on Strain Self-Limited Deformable Nanostructures toward Enhanced Field-Effect Transistors.

Strain engineering of 2D materials is capable of tuning the electrical and optical properties of the materials without introducing additional atoms. Here, a method for large-scale ultrafast strain engineering of CVD-grown 2D materials is proposed. Locally nonuniform strains are introduced through the cooperative deformation of materials and metal@metal oxide nanoparticles through cold laser shock. The tensile strain of MoS2 changes and the band gap decreases after laser shock. The mechanism of the ultrafast straining is investigated by MD simulations. MoS2 FETs were fabricated, and the field-effect mobility of devices could be increased from 1.9 to 44.5 cm2 V-1 s-1 by adjusting the strain level of MoS2. This is currently the maximum value of MoS2 FETs grown by CVD with SiO2 as the dielectric. As a large-scale and ultrafast manufacturing method, laser shock provides a universal strategy for large-scale adjustment of 2D material strain, which will help to promote the manufacturing of 2D nanoelectronic devices.

Effects of dietary phosphorus deficiency on the growth performance, hepatic lipid metabolism, and antioxidant capacity of Yellow River Carp Cyprinus carpio haematopterus.

OBJECTIVE: The study aimed to evaluate the effects of phosphorus (P) deficiency in diets on growth performance, hepatic lipid metabolism, and antioxidant capacity in Yellow River Carp Cyprinus carpio haematopterus. METHODS: In this study, 72 healthy experimental fish (initial weight = 12.0 ± 0.1 g [mean ± SE]) were randomly selected and distributed to two groups, with three replicates in each group. The groups were fed either a P-sufficient diet or a P-deficient diet for 8 weeks. RESULT: The P-deficient feed significantly decreased the specific growth rate, feed efficiency, and condition factor of Yellow River Carp. Fish that were fed the P-deficient feed demonstrated higher contents of triglyceride, total cholesterol (T-CHO), and low-density lipoprotein cholesterol in the plasma and a higher T-CHO content in the liver compared to the P-sufficient diet group. In addition, the P-deficient diet significantly reduced the catalase activity level, decreased the glutathione content, and increased the malondialdehyde content in the liver and in the plasma. Furthermore, P deficiency in the diet significantly downregulated the messenger RNA expression of nuclear erythroid 2-related factor 2 and peroxisome proliferator-activated receptor α, whereas it upregulated the messenger RNA expression of tumor necrosis factor α and fatty acid synthase in the liver. CONCLUSION: Dietary P deficiency reduced fish growth performance, induced fat deposition and oxidative stress, and impaired liver health.

Boosting CO2 Hydrogenation to Formate over Edge-Sulfur Vacancies of Molybdenum Disulfide.

Synthesis of formate from hydrogenation of carbon dioxide (CO2 ) is an atom-economic reaction but is confronted with challenges in developing high-performance non-precious metal catalysts for application of the process. Herein, we report a highly durable edge-rich molybdenum disulfide (MoS2 ) catalyst for CO2 hydrogenation to formate at 200 °C, which delivers a high selectivity of over 99 % with a superior turnover frequency of 780.7 h-1 surpassing those of previously reported non-precious metal catalysts. Multiple experimental characterization techniques combined with theoretical calculations reveal that sulfur vacancies at MoS2 edges are the active sites and the selective production of formate is enabled via a completely new water-mediated hydrogenation mechanism, in which surface OH* and H* species in dynamic equilibrium with water serve as moderate hydrogenating agents for CO2 with residual O* reduced by hydrogen. This study provides a new route for developing low-cost high-performance catalysts for CO2 hydrogenation to formate.

Identification of the Integrated Prognostic Signature Associated with Immuno-relevant Genes and Long Non-coding RNAs in Acute Myeloid Leukemia.

BACKGROUND: Like other cancers, considerable effort has been made in acute myeloid leukemia (AML) to identify prognostic genes and long noncoding RNAs (lncRNAs) with their potential clinical applications. However, to date, no integrated prognostic model has been developed that combines both gene expression and lncRNAs as a singular approach in AML. METHOD: Comprehensive bioinformatic approaches (Weighted gene co-expression network analysis, Univariate Cox regression analyses, Pearson correlation, LASSO-Cox regression, Wilcoxon test) were used to construct the signature and to define high- and low-risk groups in AML datasets. ESTIMATE and CIBERSORT algorithms were applied to investigate the potential impact of infiltrating immune cells based on the obtained signature in tumor microenvironment. In addition, gene ontology (GO) and KEGG enrichment were applied to explore the potential function of the signature. RESULTS: Herein, we focused on immune-related genes (IRGs) and immune-related long noncoding RNAs (IRlncRNAs) and constructed an integrated prognostic immunorelevant signature in AML. The obtained signature exhibit five IRGs (DAXX, PSMB8, CSRP1, RAC2 and PTPN6) and one IRlncRNA (AC080037.2) and is strictly associated with age and FAB (French-American-British classification). Importantly, the high-risk AML group (defined by the signature) correlated positively with three types of scores (immune score, stroma score, and ESTIMATE score). We also identified a few immune cells (resting mast cells and monocytes) potentially involved in the correlation between signature and survival of AML patients. The prognostic ability of the obtained signature was tested in the training cohort and then validated in both test and total cohorts. The pathway enrichment analysis confirmed the possible immune- related role of the signature. CONCLUSION: We constructed an integrated prognostic signature comprising five immune-related protein-coding genes (IRPCG) (DAXX, PSMB8, CSRP1, RAC2, and PTPN6) and one immune-related lncRNA (AC080037.2) that may serve as potential biomarkers for predicting survival and further stratifying AML patients.

Improved prediction of smoking status via isoform-aware RNA-seq deep learning models.

Most predictive models based on gene expression data do not leverage information related to gene splicing, despite the fact that splicing is a fundamental feature of eukaryotic gene expression. Cigarette smoking is an important environmental risk factor for many diseases, and it has profound effects on gene expression. Using smoking status as a prediction target, we developed deep neural network predictive models using gene, exon, and isoform level quantifications from RNA sequencing data in 2,557 subjects in the COPDGene Study. We observed that models using exon and isoform quantifications clearly outperformed gene-level models when using data from 5 genes from a previously published prediction model. Whereas the test set performance of the previously published model was 0.82 in the original publication, our exon-based models including an exon-to-isoform mapping layer achieved a test set AUC (area under the receiver operating characteristic) of 0.88, which improved to an AUC of 0.94 using exon quantifications from a larger set of genes. Isoform variability is an important source of latent information in RNA-seq data that can be used to improve clinical prediction models.

Disruption of super-enhancer-driven tumor suppressor gene RCAN1.4 expression promotes the malignancy of breast carcinoma.

BACKGROUND: Super-enhancers (SEs) play a crucial role in cancer, which is often associate with activated oncogenes. However, little is known about how SEs facilitate tumour suppression. Individuals with Down syndrome exhibit a remarkably reduced incidence of breast cancer (BC), moving the search for tumor suppressor genes on human chromosome 21 (HSA21). In this study, we aim to identify and explore potential mechanisms by which SEs are established for tumor suppressor RCAN1.4 on HSA21 in BC. METHODS: In silico analysis and immunohistochemical staining were used to assess the expression and clinical relevance of RCAN1.4 and RUNX3 in BC. Function experiments were performed to evaluate the effects of RCAN1.4 on the malignancy of breast carcinoma in vitro and in vivo. ChIP-seq data analysis, ChIP-qPCR, double-CRISPR genome editing, and luciferase reporter assay were utilized to confirm RUNX3 was involved in regulating RCAN1.4-associated SE in BC. The clinical value of co-expression of RCAN1.4 and RUNX3 was evaluated in BC patients. RESULTS: Here, we characterized RCAN1.4 as a potential tumour suppressor in BC. RCAN1.4 loss promoted tumour metastasis to bone and brain, and its overexpression inhibited tumour growth by blocking the calcineurin-NFATc1 pathway. Unexpectedly, we found RCAN1.4 expression was driven by a ~ 23 kb-long SE. RCAN1.4-SEdistal was sensitive to BRD4 inhibition, and its deletion decreased RCAN1.4 expression by over 90% and induced the malignant phenotype of BC cells. We also discovered that the binding sites in the SE region of RCAN1.4 were enriched for consensus sequences of transcription factor RUNX3. Knockdown of RUNX3 repressed the luciferase activity and also decreased H3K27ac enrichment binding at the SE region of RCAN1.4. Furthermore, abnormal SE-driven RCAN1.4 expression mediated by RUNX3 loss could be physiologically significant and clinically relevant in BC patients. Notably, we established a prognostic model based on RCAN1.4 and RUNX3 co-expression that effectively predicted the overall survival in BC patients. CONCLUSIONS: These findings reveal an important role of SEs in facilitating tumour suppression in BC. Considering that the combination of low RCAN1.4 and low RUNX3 expression has worse prognosis, RUNX3-RCAN1.4 axis maybe a novel prognostic biomarker and therapeutic target for BC patients.

Aurora kinase A stabilizes FOXM1 to enhance paclitaxel resistance in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) has a relatively poor outcome. Acquired chemoresistance is a major clinical challenge for TNBC patients. Previously, we reported that kinase-dead Aurora kinase A (Aurora-A) could effectively transactivate the FOXM1 promoter. Here, we demonstrate an additional pathway through which Aurora-A stabilizes FOXM1 by attenuating its ubiquitin in TNBC. Specifically, Aurora-A stabilizes FOXM1 in late M phase and early G1 phase of the cell cycle, which promotes proliferation of TNBC cells. Knock-down of Aurora-A significantly suppresses cell proliferation in TNBC cell lines and can be rescued by FOXM1 overexpression. We observe that paclitaxel-resistant TNBC cells exhibit high expression of Aurora-A and FOXM1. Overexpression of Aurora-A offers TNBC cells an additional growth advantage and protection against paclitaxel. Moreover, Aurora-A and FOXM1 could be simultaneously targeted by thiostrepton. Combination of thiostrepton and paclitaxel treatment reverses paclitaxel resistance and significantly inhibits cell proliferation. In conclusion, our study reveals additional mechanism through which Aurora-A regulates FOXM1 and provides a new therapeutic strategy to treat paclitaxel-resistant triple-negative breast cancer.

Imbalance in the ratio of CpG and polyG contributes to impaired interferon-α expression.

The secretion of interferon-α (IFN-α) is impaired during hepatitis B virus (HBV) infection. DNA sequences purified from distinct viruses, for example, HBV versus members of Herpesviridae, have been shown to differ in their IFN-α signaling properties. The present study found that DNA from HBV inhibited, while DNA from members of Herpesviridae induced, the expression of IFN-α. Furthermore, stimulatory cytosine-phosphate-guanosine (CpG) sequences derived from these DNA viruses could induce the secretion of IFN-α, while inhibitory guanosine-rich oligodeoxynucleoti (polyG) oligonucleotide sequences derived from these DNA viruses could inhibit CpG-induced IFN-α secretion. Using a computational analysis of genomic DNA sequences, the discrimination between the genomes of HBV and those of other DNA viruses that can also cause inflammation of the liver is based on different frequencies of the CpG and polyG motifs. The underrepresentation of stimulatory CpG motifs and overrepresentation of inhibitory polyG motifs were documented in HBV genomes, whereas the DNA from other viral genomes displayed the opposite trend. Moreover, it was demonstrated that HBV could suppress the activation of IFN-α via its own DNA through the high proportion of polyG motifs. To our knowledge, this is the first demonstration of a specific role for polyG motifs in the inhibition of the IFN-α response following DNA virus infection.

Boron ink assisted in situ boron nitride coatings for anti-oxidation and anti-corrosion applications.

Graphene as a coating material that shows high impermeability as an excellent barrier in oxidation and corrosion protection has been reported to be less stable at elevated temperature. Sometimes the formed galvanic cell between the graphene and protective surface will even increase the corrosion speed. In comparison, boron nitride (BN), which shows the same impermeability with graphene, is believed to be a better coating material with its superior thermal and chemical inertness. In this study, an in situ synthesis of BN coatings, grown by boron ink, on both carbon and Cu for anti-oxidation and anti-corrosion purposes has been demonstrated. Thermogravimetric analysis and electrochemical analysis reveal that the BN coatings can effectively prevent the carbon from being oxidized at high temperature in air and adequately slow down the corrosion rate of Cu in sodium chloride solution, respectively. These results indicate that boron ink assisted in situ BN coating has high potential in the applications of oxidation and corrosion protection.

Estimating PM2.5 Concentrations Based on MODIS AOD and NAQPMS Data over Beijing⁻Tianjin⁻Hebei.

Accurately estimating fine ambient particulate matter (PM2.5) is important to assess air quality and to support epidemiological studies. To analyze the spatiotemporal variation of PM2.5 concentrations, previous studies used different methodologies, such as statistical models or neural networks, to estimate PM2.5. However, there is little research on full-coverage PM2.5 estimation using a combination of ground-measured, satellite-estimated, and atmospheric chemical model data. In this study, the linear mixed effect (LME) model, which used the aerosol optical depth (AOD) from the Moderate Resolution Imaging Spectroradiometer (MODIS), meteorological data, normalized difference vegetation index (NDVI), and elevation data as predictors, was fitted for 2017 over Beijing⁻Tianjin⁻Hebei (BTH). The LME model was used to calibrate the PM2.5 concentration using the nested air-quality prediction modeling system (NAQPMS) simulated with ground measurements. The inverse variance weighting (IVW) method was used to fuse satellite-estimated and model-calibrated PM2.5. The results showed a strong agreement with ground measurements, with an overall coefficient (R²) of 0.78 and a root-mean-square error (RMSE) of 26.44 µg/m³ in cross-validation (CV). The seasonal R² values were 0.75, 0.62, 0.80, and 0.78 in the spring, summer, autumn, and winter, respectively. The fusion results supplement the lack of satellite estimates and can capture more detailed information than the NAQPMS model. Therefore, the results will be helpful for pollution process analyses and health-related studies.

Satellite-Based Estimation of Hourly PM2.5 Concentrations Using a Vertical-Humidity Correction Method from Himawari-AOD in Hebei.

Abstract: Particulate matter with an aerodynamic diameter less than 2.5 µm (PM2.5) is related to various adverse health effects. Ground measurements can yield highly accurate PM2.5 concentrations but have certain limitations in the discussion of spatial-temporal variations in PM2.5. Satellite remote sensing can obtain continuous and long-term coverage data, and many previous studies have demonstrated the relationship between PM2.5 and AOD (aerosol optical depth) from theoretical analysis and observation. In this study, a new aerosol product with a high spatial-temporal resolution retrieved from the AHI (the Advance Himawari Imager) was obtained using a vertical-humidity correction method to estimate hourly PM2.5 concentrations in Hebei. The hygroscopic growth factor (fRH) was fitted at each site (in a total of 137 matched sites). Meanwhile, assuming that there was little change in fRH at a certain scale, the nearest fRH of each pixel was determined to calculate PM2.5 concentrations. Compared to the correlation between AOD and PM2.5, the relationship between the "dry" mass extinction efficiency obtained by vertical-humidity correction and the ground-measured PM2.5 significantly improved, with r coefficient values increasing from 0.19⁻0.47 to 0.61⁻0.76. The satellite-estimated hourly PM2.5 concentrations were consistent with the ground-measured PM2.5, with a high r (0.8 ± 0.07) and a low RMSE (root mean square error, 30.4 ± 5.5 µg/m³) values, and the accuracy in the afternoon (13:00⁻16:00) was higher than that in the morning (09:00⁻12:00). Meanwhile, in a comparison of the daily average PM2.5 concentrations of 11 sites from different cities, the r values were approximately 0.91 ± 0.03, and the RMSEs were between 13.94 and 31.44 µg/m³. Lastly, pollution processes were analyzed, and the analysis indicated that the high spatial-temporal resolution of the PM2.5 data could continuously and intuitively reflect the characteristics of regional pollutants (such as diffusion and accumulation), which is of great significance for the assessment of regional air quality.