Cannabidiol protects against acute aortic dissection by inhibiting macrophage infiltration and PMAIP1-induced vascular smooth muscle cell apoptosis.

Acute aortic dissection (AAD) progresses rapidly and is associated with high mortality; therefore, there remains an urgent need for pharmacological agents that can protect against AAD. Herein, we examined the therapeutic effects of cannabidiol (CBD) in AAD by establishing a suitable mouse model. In addition, we performed human AAD single-cell RNA sequencing and mouse AAD bulk RNA sequencing to elucidate the potential underlying mechanism of CBD. Pathological assays and in vitro studies were performed to verify the results of the bioinformatic analysis and explore the pharmacological function of CBD. In a ß-aminopropionitrile (BAPN)-induced AAD mouse model, CBD reduced AAD-associated morbidity and mortality, alleviated abnormal enlargement of the ascending aorta and aortic arch, and suppressed macrophage infiltration and vascular smooth muscle cell (VSMC) apoptosis. Bioinformatic analysis revealed that the pro-apoptotic gene PMAIP1 was highly expressed in human and mouse AAD samples, and CBD could inhibit Pmaip1 expression in AAD mice. Using human aortic VSMCs (HAVSMCs) co-cultured with M1 macrophages, we revealed that CBD alleviated HAVSMCs mitochondrial-dependent apoptosis by suppressing the BAPN-induced overexpression of PMAIP1 in M1 macrophages. PMAIP1 potentially mediates HAVSMCs apoptosis by regulating Bax and Bcl2 expression. Accordingly, CBD reduced AAD-associated morbidity and mortality and mitigated the progression of AAD in a mouse model. The CBD-induced effects were potentially mediated by suppressing macrophage infiltration and PMAIP1 (primarily expressed in macrophages)-induced VSMC apoptosis. Our findings offer novel insights into M1 macrophages and HAVSMCs interaction during AAD progression, highlighting the potential of CBD as a therapeutic candidate for AAD treatment.

Unveiling the therapeutic potential of IHMT-337 in glioma treatment: targeting the EZH2-SLC12A5 axis.

Glioma is the most common malignant tumor of the central nervous system, with EZH2 playing a crucial regulatory role. This study further explores the abnormal expression of EZH2 and its mechanisms in regulating glioma progression. Additionally, it was found that IHMT-337 can potentially be a therapeutic agent for glioma. The prognosis, expression, and localization of EZH2 were determined using bioinformatics, IHC staining, Western blot (WB) analysis, and immunofluorescence (IF) localization. The effects of EZH2 on cell function were assessed using CCK-8 assays, Transwell assays, and wound healing assays. Public databases and RT-qPCR were utilized to identify downstream targets. The mechanisms regulating these downstream targets were elucidated using MS-PCR and WB analysis. The efficacy of IHMT-337 was demonstrated through IC50 measurements, WB analysis, and RT-qPCR. The effects of IHMT-337 on glioma cells in vitro were evaluated using Transwell assays, EdU incorporation assays, and flow cytometry. The potential of IHMT-337 as a treatment for glioma was assessed using a blood-brain barrier (BBB) model and an orthotopic glioma model. Our research confirms significantly elevated EZH2 expression in gliomas, correlating with patient prognosis. EZH2 facilitates glioma proliferation, migration, and invasion alongside promoting SLC12A5 DNA methylation. By regulating SLC12A5 expression, EZH2 activates the WNK1-OSR1-NKCC1 pathway, enhancing its interaction with ERM to promote glioma migration. IHMT-337 targets EZH2 in vitro to inhibit WNK1 activation, thereby suppressing glioma cell migration. Additionally, it inhibits cell proliferation and arrests the cell cycle. IHMT-337 has the potential to cross the BBB and has successfully inhibited glioma progression in vivo. This study expands our understanding of the EZH2-SLC12A5 axis in gliomas, laying a new foundation for the clinical translation of IHMT-337 and offering new insights for precision glioma therapy.

Multiple-access ultrastable frequency dissemination based on optical frequency combs via a fiber link.

We demonstrate an optical fiber-based, multiple-access frequency transmission using two optical frequency combs. The experimental results using the Allan deviation analysis show that with the phase compensation technique, the frequency instabilities at the remote site are 8.7 × 10-15/1 s and 1.0 × 10-17/103 s, and at the accessing node along the fiber link, the frequency instabilities are 6.9 × 10-15/1 s and 1.1 × 10-17/103 s. Similarly, the power spectral density of phase noise was analyzed in the frequency domain. These experimental results demonstrate that the compensation scheme improved the performance by two to three orders of magnitude. Thus, the proposed frequency transmission technique has potential application for disseminating ultrastable frequency references in the optical fiber network.

Development of a nomogram based on the clinicopathological and CT features to predict the survival of primary pulmonary lymphoepithelial carcinoma patients.

BACKGROUND: The aim of this study was to develop a nomogram by combining chest computed tomography (CT) images and clinicopathological predictors to assess the survival outcomes of patients with primary pulmonary lymphoepithelial carcinoma (PLEC). METHODS: 113 patients with stage I-IV primary PLEC who underwent treatment were retrospectively reviewed. The Cox regression analysis was performed to determine the independent prognostic factors associated with patient's disease-free survival (DFS) and cancer-specific survival (CSS). Based on results from multivariate Cox regression analysis, the nomograms were constructed with pre-treatment CT features and clinicopathological information, which were then assessed with respect to calibration, discrimination and clinical usefulness. RESULTS: Multivariate Cox regression analysis revealed the independent prognostic factors for DFS were surgery resection and hilar and/or mediastinal lymphadenopathy, and that for CSS were age, smoking status, surgery resection, tumor site in lobe and necrosis. The concordance index (C­index) of nomogram for DFS and CSS were 0.777 (95% CI: 0.703-0.851) and 0.904 (95% CI: 0.847-0.961), respectively. The results of the time­dependent C­index were internally validated using a bootstrap resampling method for DFS and CSS also showed that the nomograms had a better discriminative ability. CONCLUSIONS: We developed nomograms based on clinicopathological and CT factors showing a good performance in predicting individual DFS and CSS probability among primary PLEC patients. This prognostic tool may be valuable for clinicians to more accurately drive treatment decisions and individualized survival assessment.

Molecular Design of Functional Polymers for Silica Scale Inhibition.

Silica polymerization, which involves the condensation reaction of silicic acid, is a fundamental process with wide-ranging implications in biological systems, material synthesis, and scale formation. The formation of a silica-based scale poses significant technological challenges to energy-efficient operations in various industrial processes, including heat exchangers and water treatment membranes. Despite the common strategy of applying functional polymers for inhibiting silica polymerization, the underlying mechanisms of inhibition remain elusive. In this study, we synthesized a series of nitrogen-containing polymers as silica inhibitors and elucidated the role of their molecular structures in stabilizing silicic acids. Polymers with both charged amine and uncharged amide groups in their backbones exhibit superior inhibition performance, retaining up to 430 ppm of reactive silica intact for 8 h under neutral pH conditions. In contrast, monomers of these amine/amide-containing polymers as well as polymers containing only amine or amide functionalities present insignificant inhibition. Molecular dynamics simulations reveal strong binding between the deprotonated silicic acid and a polymer when the amine groups in the polymer are protonated. Notably, an extended chain conformation of the polymer is crucial to prevent proximity between the interacting monomeric silica species, thereby facilitating effective silica inhibition. Furthermore, the hydrophobic nature of alkyl segments in polymer chains disrupts the hydration shell around the polymer, resulting in enhanced binding with ionized silicic acid precursors compared to monomers. Our findings provide novel mechanistic insights into the stabilization of silicic acids with functional polymers, highlighting the molecular design principles of effective inhibitors for silica polymerization.

Short-term reproductive outcomes analysis and prediction of the modified uterine stent treatment for mild to moderate intrauterine adhesions: experience at a single institution.

BACKGROUND: To evaluate the efficacy of modified uterine stent in the treatment of mild-to-moderate intrauterine adhesions and explore the relative indicators affecting prognosis prediction. METHODS: A total of 115 patients with mild-to-moderate intrauterine adhesions received a modified uterine stent placement after hysteroscopy adhesiolysis. The second-look hysteroscopy operated after 3 months surgery, and the third-look hysteroscopy operated after 6 months surgery if necessary. The stent was removed when the cavity shape was repaired, then the reproductive outcomes were followed up one year. RESULTS: Menstrual blood volume, endometrial thickness and volume had increased significantly after 3 months surgery. The rates of cavity repaired were 86.96% (100/115) after 3 months surgery and 100% (115/115) after 6 months surgery cumulatively. Endometrial thickness after 3-months surgery was positively associated with uterine cavity shape repaired (P<0.01). The receive operating characteristic (ROC) curve showed the rate of uterine cavity shape repaired predicted by the model was 0.92, based on the endometrial thickness after 3-months surgery. The rate of pregnancy was 86.09% (99/115) in one year, while the rate of miscarriage accounted for 26.26% (26/99). The median time interval between stent removal and subsequent conception was 3 months. It showed adhesion recurrence was the risk factor for subsequent pregnancy (P<0.01). CONCLUSIONS: A modified uterine stent placement under hysteroscopy was an effective approach for mild-to-moderate intrauterine adhesions, which is easy to operate and worthy for clinical promotion. Endometrial thickness measured by ultrasonography probably has predictive value in adhesion recurrence and subsequent pregnancy. TRIAL REGISTRATION: ChiCTR2100051524. Date of registration (retrospectively registered): 26/09/2021.

Fibrin aggravates periodontitis through inducing NETs formation from mitochondrial DNA.

OBJECTIVES: This study investigated the role of fibrin on neutrophil extracellular traps (NETs) formation from neutrophils and to elucidate the involvement of mitochondria in NETs formation during periodontitis. MATERIALS AND METHODS: Plasminogen-deficient (Plg-/-) mice were employed to evaluate the effects of fibrin deposition on inflammation, bone resorption, and neutrophil infiltration in periodontal tissues. In addition, in vitro tests evaluated fibrin's impact on neutrophil-driven inflammation. Mitochondrial reactive oxygen species (mtROS) levels within neutrophils were quantified utilizing flow cytometry and immunofluorescence in vitro. Furthermore, the anti-inflammatory properties of the mtROS scavenger, Mito-TEMPO, were confirmed to regulate the NET formation in vitro and in vivo. RESULTS: Plasminogen deficiency resulted in increased fibrin deposition, neutrophil infiltration, inflammatory factors concentration, and alveolar bone resorption in periodontal tissues. After neutrophils were treated by fibrin in vitro, the expression of inflammatory factors, the formation of mtROS, and NETs enriched in mitochondrial DNA (mtDNA) were upregulated, which were reversed by Mito-TEMPO in vitro. Moreover, Mito-TEMPO alleviated inflammation in Plg-/- mice. CONCLUSIONS: This study showed that fibrin deposition in gingiva induced the NET formation in Plg-/- mice, in which the DNA in NETs was from mitochondria depending on increasing mtROS.

FADD amplification is associated with CD8+ T-cell exclusion and malignant progression in HNSCC.

OBJECTIVE: This study aimed to clarify the relationship between FADD amplification and overexpression and the tumor immune microenvironment. METHODS: Immunohistochemical staining and bioanalysis were used to analyze the association between FADD expression in tumor cells and cells in tumor microenvironment. RNA-seq analysis was used to detect the differences in gene expression upon FADD overexpression. Flow cytometry and multicolor immunofluorescence staining (mIHC) were used to detect the differences in CD8+ T-cell infiltration in FADD-overexpressed cells or tumor tissues. RESULTS: Overexpression of FADD significantly promoted tumor growth. Cells with high FADD expression presented high expression of CD276 and FGFBP1 and low expression of proinflammatory factors (such as IFIT1-3 and CXCL8), which reduced the percentage of CD8+ T cells and created a "cold tumor" immune microenvironment, thus promoting tumor progression. In vivo and in vitro experiment confirmed that tumor tissues with excessive FADD expression exhibited CD8+ T-cell exclusion in the microenvironment. CONCLUSION: Our preliminary investigation has discovered the association between FADD expression and the immunosuppressive microenvironment in HNSCC. Due to the high frequent amplification of the chromosomal region 11q13.3, where FADD is located, targeting FADD holds promise for improving the immune-inactive state of tumors, subsequently inhibiting HNSCC tumor progression.

Integrative analysis of bulk RNA-seq and scRNA-seq data indicates the prognostic and immunologic values of SERPINH1 in glioma.

BACKGROUND: SERPINH1 is abnormally expressed in multiple cancers and is associated with malignant progression. However, few reports detail its role in the etiopathogenesis of glioma. Hence, the aim of this article was to investigate the potential value of SERPINH1 in glioma using an integrative analysis. METHODS: Data of RNA-seq and scRNA-seq was obtained and evaluated using online databases. The expression of SERPINH1 was confirmed by qRT-PCR and immunohistochemistry. The prognostic value of SERPINH1 was evaluated using univariate and multivariate Cox regression analyses. SERPINH1-related signaling pathways and the interaction of SERPINH1 with immunity were also investigated. RESULTS: SERPINH1 exhibited a markedly elevated expression in glioma compared to normal brain tissues in the online databases. Similar results were confirmed by qRT-PCR and immunohistochemistry. SERPINH1 was found to be an independent prognosis factor, and high expression of SERPINH1 indicated poor survival. Moreover, a nomogram was constructed to predict prognosis more accurately and intuitively. GSEA analysis showed that SERPINH1 was involved in seven signaling pathways, including JAK-STAT pathway. Further analysis indicated SERPINH1 was significantly associated with immunity, especially in low-grade glioma. Additionally, an examination of scRNA-seq data revealed that SERPINH1 was primarily expressed in T cells of the CD4+ and CD8+ subsets. CONCLUSIONS: SERPINH1 is a key biomarker of glioma prognosis and is immunologically relevant, which provides additional options for targeted therapy of glioma.

H3.3B controls aortic dissection progression by regulating vascular smooth muscle cells phenotypic transition and vascular inflammation.

Aortic dissection is a devastating cardiovascular disease with a high lethality. Histone variants maintain the genomic integrity and play important roles in development and diseases. However, the role of histone variants in aortic dissection has not been well identified. In the present study, H3f3b knockdown reduced the synthetic genes expression of VSMCs, while overexpressing H3f3b exacerbated the cellular immune response of VSMCs induced by inflammatory cytokines. Combined RNA-seq and ChIP-seq analyses revealed that histone variant H3.3B directly bound to the genes related to extracellular matrix, VSMC synthetic phenotype, cytokine responses and TGFß signaling pathway, and regulated their expressions. In addition, VSMC-specific H3f3b knockin aggravated aortic dissection development in mice, while H3f3b knockout significantly reduced the incidence of aortic dissection. In term of mechanisms, H3.3B regulated Spp1 and Ccl2 genes, inducing the apoptosis of VSMCs and recruiting macrophages. This study demonstrated the vital roles of H3.3B in phenotypic transition of VSMCs, loss of media VSMCs, and vascular inflammation in aortic dissection.

Chemical Mapping of Excitons in Halide Double Perovskites.

Halide double perovskites comprise an emerging class of semiconductors with tremendous chemical and electronic diversity. While their band structure features can be understood from frontier-orbital models, chemical intuition for optical excitations remains incomplete. Here, we use ab initio many-body perturbation theory within the GW and the Bethe-Salpeter equation approach to calculate excited-state properties of a representative range of Cs2BB'Cl6 double perovskites. Our calculations reveal that double perovskites with different combinations of B and B' cations display a broad variety of electronic band structures and dielectric properties and form excitons with binding energies ranging over several orders of magnitude. We correlate these properties with the orbital-induced anisotropy of charge-carrier effective masses and the long-range behavior of the dielectric function by comparing them with the canonical conditions of the Wannier-Mott model. Furthermore, we derive chemically intuitive rules for predicting the nature of excitons in halide double perovskites using computationally inexpensive density functional theory calculations.

Circular RNA 0001789 sponges miR-140-3p and regulates PAK2 to promote the progression of gastric cancer.

BACKGROUND: Gastric cancer (GC) is the third-leading cause of cancer-associated mortalities globally. The deregulation of circular RNAs (circRNAs) and microRNAs (miRNAs or miRs) is widely implicated in the pathogenesis and progression of different cancer types. METHODS: The expression profiling of circRNAs in GC is required to identify crucial circRNAs as biomarkers or therapeutic targets. In the present study, a published circRNA microarray dataset was used to identify differentially expressed circRNAs between GC tissues and normal gastric mucosa tissues. Reverse transcription-quantitative PCR was performed to validate the expression of circ_0001789. Fisher's exact test, receiver operating characteristic curve and Kaplan-Meier plots were employed to analyze the clinical significance of circ_0001789. The miRNA targets of circ_0001789 were predicted using an online database, and their functional interaction was further confirmed by RNA pull-down, RNA immunoprecipitation and dual luciferase reporter assays. Transwell assays were conducted to investigate the biological functions of circ_0001789, miR-140-3p and p21 activated kinase 2 (PAK2) in the migration and invasion of GC cells. A xenograft mouse model was established to validate the role of circ_0001789 in the tumorigenesis of GC cells. RESULTS: circ_0001789 was identified as a highly expressed circRNA in GC tissues versus normal gastric mucosa tissues. Silencing circ_0001789 attenuated the malignancy of GC cells, and exosomal circ_0001789 was sufficient to regulate the malignant phenotype of GC cells. miR-140-3p was further identified as a downstream target of circ_0001789, which showed a negative correlation with circ_0001789 expression in GC tissues. Overexpression of miR-140-3p suppressed cell migration, invasion and epithelial-mesenchymal transition in GC cells. PAK2 was identified as the target of miR-140-3 to mediate the malignant phenotype of GC cells. CONCLUSION: The present data suggested that the upregulation of circ_0001789 was associated with the progression of GC and with poor prognosis in patients with GC, and that miR-140-3p/PAK2 served as the downstream axis to mediate the oncogenic effect of circ_0001789.

Spectral Clustering Community Detection Algorithm Based on Point-Wise Mutual Information Graph Kernel.

To address the problem that traditional spectral clustering algorithms cannot obtain the complete structural information of networks, this paper proposes a spectral clustering community detection algorithm, PMIK-SC, based on the point-wise mutual information (PMI) graph kernel. The kernel is constructed according to the point-wise mutual information between nodes, which is then used as a proximity matrix to reconstruct the network and obtain the symmetric normalized Laplacian matrix. Finally, the network is partitioned by the eigendecomposition and eigenvector clustering of the Laplacian matrix. In addition, to determine the number of clusters during spectral clustering, this paper proposes a fast algorithm, BI-CNE, for estimating the number of communities. For a specific network, the algorithm first reconstructs the original network and then runs Monte Carlo sampling to estimate the number of communities by Bayesian inference. Experimental results show that the detection speed and accuracy of the algorithm are superior to other existing algorithms for estimating the number of communities. On this basis, the spectral clustering community detection algorithm PMIK-SC also has high accuracy and stability compared with other community detection algorithms and spectral clustering algorithms.

Serum metabolomic profiling for patients with adenocarcinoma of the esophagogastric junction.

INTRODUCTION: The incidence of adenocarcinoma in the esophagogastric junction (AEG) has increased in the recent years. AEG is reported to have a worse prognosis compared with tumor confined to the stomach (non-AEG). Although the metabolic changes of non-AEG have been investigated in extensive studies, little effort focused on the metabolic profiling of AEG serum. OBJECTIVES: Here we report an untargeted gas chromatography-mass spectrometry (GC-MS) method to explore the abnormal metabolism underlying AEG. METHODS: GC-MS-based untargeted metabolomics approach combined with multivariate statistical analyses were used to study the metabolic profiling of serum samples from AEG patients (n = 70), non-AEG patients (n = 70) and health controls (n = 71). RESULTS: A novel serum metabolic profiling of 18 metabolites from patients of AEG and non-AEG was indicated, in comparison with health controls. Moreover, AEG and non-AEG were also well-classified with 9 distinguishing metabolites including hypoxanthine, alanine, proline, pyroglutamate, glycine, lactate, succinic acid, glutamate and kynurenine, which produced a discriminatory model with an area under the Receiver Operating Characteristic (ROC) curve of 0.852, suggesting a distinct metabolic signature of AEG. Importantly, lactate and glutamate disclosed outcome-prediction values by multivariate cox-proportional hazard model and Kaplan-Meier method based on follow-up information for 2-5 years. CONCLUSION: This is the first metabolomics study to identify serum metabolic signature of AEG. The distinguishing metabolites show a promising application on clinical diagnose and outcome prediction, and allow us to unveil several key metabolic variations coexisting in AEG, which may aid to understand the underlying metabolic mechanisms.

EZH2 is a potential prognostic predictor of glioma.

The enhancer of zeste homologue 2 (EZH2) is a histone H3 lysine 27 methyltransferase that promotes tumorigenesis in a variety of human malignancies by altering the expression of tumour suppressor genes. To evaluate the prognostic value of EZH2 in glioma, we analysed gene expression data and corresponding clinicopathological information from the Chinese Glioma Genome Atlas, the Cancer Genome Atlas and GTEx. Increased expression of EZH2 was significantly associated with clinicopathologic characteristics and overall survival as evaluated by univariate and multivariate Cox regression. Gene Set Enrichment Analysis revealed an association of EZH2 expression with the cell cycle, DNA replication, mismatch repair, p53 signalling and pyrimidine metabolism. We constructed a nomogram for prognosis prediction with EZH2, clinicopathologic variables and significantly correlated genes. EZH2 was demonstrated to be significantly associated with several immune checkpoints and tumour-infiltrating lymphocytes. Furthermore, the ESTIMATE and Timer Database scores indicated correlation of EZH2 expression with a more immunosuppressive microenvironment for glioblastoma than for low grade glioma. Overall, our study demonstrates that expression of EZH2 is a potential prognostic molecular marker of poor survival in glioma and identifies signalling pathways and immune checkpoints regulated by EHZ2, suggesting a direction for future application of immune therapy in glioma.

Exosomal miR-409-3p secreted from activated mast cells promotes microglial migration, activation and neuroinflammation by targeting Nr4a2 to activate the NF-κB pathway.

OBJECTIVE: Neuroinflammation plays a critical role in central nervous system diseases. Exosomal miRNAs released from various cells are implicated in cell-to-cell communication. Prior studies have placed substantial emphasis on the role of cytokines in mast cell-microglia interactions during neuroinflammation. However, it has never been clearly determined whether exosomal miRNAs participate in the interaction between mast cells and microglia and thus mediate neuroinflammation. METHODS: The characteristics of exosomes isolated from cell culture supernatants were confirmed by transmission electron microscopy (TEM), nanoparticle-tracking analysis (NTA) and Western blot. The transfer of PKH67-labelled exosomes and Cy3-labelled miR-409-3p was observed by fluorescence microscopy. Migration and activation of murine BV-2 microglial cells were evaluated through Transwell assays and immunofluorescence staining for Iba1 and CD68. CD86, IL-1ß, IL-6 and TNF-α were assessed via qRT-PCR and ELISA. MiR-409-3p was detected by qRT-PCR. Nr4a2 and NF-κB levels were measured by western blot. Regulatory effects were identified by luciferase reporter assays. RESULTS: Lipopolysaccharide (LPS)-stimulated murine P815 mast cells secreted exosomes that were efficiently taken up by murine BV-2 cells, which promoted murine BV-2 cell migration and activation. LPS-P815 exosomes increased the CD86, IL-1ß, IL-6 and TNF-α levels in murine BV-2 microglia. Furthermore, activated mast cells delivered exosomal miR-409-3p to murine BV-2 microglia. Upregulated miR-409-3p promoted murine BV-2 microglial migration, activation and neuroinflammation by targeting Nr4a2 to activate the NF-κB pathway. CONCLUSION: Exosomal miR-409-3p secreted from activated mast cells promotes microglial migration, activation and neuroinflammation by targeting Nr4a2 to activate the NF-κB pathway, which provides evidence that not only cytokines but also exosomal miRNAs participate in neuroinflammation. In the future, targeting exosomal miRNAs may provide new insights into neuroinflammation.

Delineation of colorectal cancer ligand-receptor interactions and their roles in the tumor microenvironment and prognosis.

BACKGROUND: Immunotherapies targeting ligand-receptor interactions (LRIs) are advancing rapidly in the treatment of colorectal cancer (CRC), and LRIs also affect many aspects of CRC development. However, the pattern of LRIs in CRC and their effect on tumor microenvironment and clinical value are still unclear. METHODS: We delineated the pattern of LRIs in 55,539 single-cell RNA sequencing (scRNA-seq) samples from 29 patients with CRC and three bulk RNA-seq datasets containing data from 1411 CRC patients. Then the influence of tumor microenvironment, immunotherapy and prognosis of CRC patients were comprehensively investigated. RESULTS: We calculated the strength of 1893 ligand-receptor pairs between 25 cell types to reconstruct the spatial structure of CRC. We identified tumor subtypes based on LRIs, revealed the relationship between the subtypes and immunotherapy efficacy and explored the ligand-receptor pairs and specific targets affecting the abundance of tumor-infiltrating lymphocytes. Finally, a prognostic model based on ligand-receptor pairs was constructed and validated. CONCLUSION: Overall, through the comprehensive and in-depth investigation of the existing ligand-receptor pairs, this study provides new ideas for CRC subtype classification, a new risk screening tool for CRC patients, and potential ligand-receptor pair targets and pathways for CRC therapy.

Porous 3D graphene aerogel co-doped with nitrogen and sulfur for high-performance supercapacitors.

Heteroatom-doped carbon materials with a high specific area, a well-defined porous structure is important to high-performance supercapacitors (SCs). Here, S and N co-doped three-dimensional porous graphene aerogel (NS-3DPGHs) have been synthesized in a facile and efficient self-assembly process with thiourea acting as the reducing and doping agent solution. Operating as a SC electrode, fabricated co-doping graphene, i.e. the sample of NS-3DPGH-150 exhibits the highest specific capacitance of 412.9 F g-1 under 0.5 A g-1 and prominent cycle stabilization with 96.4% capacitance retention in the back of 10 000 cycles. Furthermore, based on NS-3DPGH-150, the symmetrical supercapacitor as-prepared in 6 M KOH displays a superior energy density of 12.9 Wh kg-1 under the power density of 249 W kg-1. Hence, NS-3DPGHs could be considered as an excellent candidate for SCs.

Flexible all-solid-state supercapacitors based on PPy/rGO nanocomposite on cotton fabric.

Polypyrrole (PPy) has high electrochemical activity and low cost, so it has great application prospects in wearable supercapacitors. Herein, we have successfully prepared polypyrrole/reduced graphene oxide (PPy/rGO) nanocomposite cotton fabric (NCF) by chemical polymerization, which exhibits splendid electrochemical performance compared with the individual. The addition of rGO can block the deformation of PPy caused by the expansion and contraction. The as-prepared PPy-0.5/rGO NCF electrode exhibits the brilliant specific capacitance (9300 mF cm-2at 1 mA cm-2) and the capacitance retention with 94.47% after 10 000 cycles. At the same time, the superior capacitance stability under different bending conditions and reuse capability have been achieved. All-solid-state supercapacitor has high energy density of 167µWh cm-2with a power density of 1.20 mW cm-2. Therefore, the PPy-0.5/rGO NCF electrode has a broad application prospect in high-performance flexible supercapacitor fabric electrode.

Recent Advances in Living Cationic Polymerization with Emerging Initiation/Controlling Systems.

While the conventional living cationic polymerization (LCP) provided opportunities to synthesizing well-defined polymers with predetermined molecular weights, desirable chemical structures and narrow dispersity, it is still important to continuously innovate new synthetic methods to meet the increasing requirements in advanced material engineering. Consequently, a variety of novel initiation/controlling systems have be demonstrated recently, which have enabled LCP with spatiotemporal control, broadened scopes of monomers and terminals, more user-friendly operations and reaction conditions, as well as improved thermomechanical properties for obtained polymers. In this work, recent advances in LCP is summarized with emerging initiation/controlling systems, including chemical-initiated/controlled cationic reversible addition-fragmentation chain transfer (RAFT) polymerization, photoinitiated/controlled LCP, electrochemical-controlled LCP, thionyl/selenium halide-initiated LCP, organic acid-assisted LCP, and stereoselective LCP. It is hoped that this summary will provide useful knowledge to people in related fields and stimulate new ideas to promote the development and application of LCP in both academia and industry.