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Microscale damage, including cracks and electrical trees, is inevitably generated in the polymer insulation materials used in the packaging of power equipment and power electronic devices during long-term operation, which leads to premature insulation failure or even widespread power outages. Self-healing insulation materials are the most promising way to solve this problem. However, the mechanical/electrical strength or the dimensional stability of the materials could be sacrificed during the repair process, which has limited their application as insulation materials. In this study, we report an intrinsic self-healing epoxy resin based on reversible anthracene photodimerization (ISEP-RAP) that remains mechanically robust while ensuring efficient healing via a reversible reaction. The damaged area is decrosslinked by 254 nm UV and thermal excitation, which accelerates the molecular chain diffusion to the damaged area to fill and repair the damaged channels. The ISEP-RAP is recrosslinked by 365 nm UV to restore the mechanical and electrical properties after self-healing. Due to the combined action of the epoxy-amine permanent crosslinking sites and the anthracene reversible crosslinking sites, high crosslinked ISEP-RAP possesses excellent tensile and dielectric strength similar to that of standard epoxy resin and a lower permittivity constant. Importantly, the decrosslinked ISEP-RAP still possesses sufficiently high strength to keep the macrostructure unchanged. ISEP-RAP achieves high-efficiency, repeatable, non-contact intrinsic self-healing of scratches and electrical trees with whole-process dimensional stability. This work provides a new method for intrinsic self-healing in mechanically robust insulation materials to eliminate microdamage with repeatability, high reliability, and high efficiency. [ABSTRACT FROM AUTHOR]

The development of high‐precision, non‐destructive, and three‐dimensional (3D) in situ imaging of micro‐scale damage inside polymers is extremely challenging. Recent reports suggest that 3D imaging technology based on micro‐CT technology causes irreversible damage to materials and is ineffective for many elastomeric materials. In this study, it is discovered that electrical trees inside silicone gel induced by an applied electric field can induce a self‐excited fluorescence effect. Based on this, high‐precision, non‐destructive, and 3D in situ fluorescence imaging of polymer damages is successfully achieved. Compared with the current methods, the fluorescence microscopic imaging method enables slicing of the sample in vivo with high‐precision operation, realizing the precise positioning of the damaged area. This pioneering discovery paves the way for high‐precision, non‐destructive, and 3D in situ imaging of polymer internal damage, which can solve the problem of internal damage imaging in insulating materials and precision instruments. [ABSTRACT FROM AUTHOR]

Myelodysplastic syndrome (MDS) is a clonal bone marrow disorder with a high propensity to develop into acute myeloid leukemia (AML). Although abnormal microRNA expression has been implicated in MDS, the exact role of miR-181a-2-3p has not been entirely elucidated. Here, we investigated miR-181a-2-3p levels in bone marrow (BM), and described its utility as a potential indicator for MDS diagnosis and prognosis. We evaluated miR-181a-2-3p expression in BM samples of 54 newly diagnosed MDS cases, 16 sAML patients and 32 healthy donors and then assessed its association with clinical characteristics and its potential value for MDS diagnosis and prognosis. Compared with healthy controls, miR-181a-2-3p levels were decreased in the total cohort of MDS patients. Additionally, in MDS patients with secondary AML (sAML), miR-181a-2-3p was over-expressed relative to levels in those without this form. The areas under the curve of receiver operating characteristic curves were 0.700 and 0.750 to distinguish MDS patients from controls and sAML from newly diagnosed MDS, respectively. Kaplan–Meier analysis showed a positive correlation between miR-181a-2-3p expression and overall survival (OS). Further, multivariate analysis indicated that miR-181a-2-3p was an independent prognostic index for MDS with respect to OS. Decreased miR-181a-2-3p expression in MDS patients may be considered as one of the underlying markers reflecting MDS progression and prognosis. [ABSTRACT FROM AUTHOR]

To determine the expression level of RAG1 and its clinical significance in myelodysplastic syndromes (MDS). To explore the candidate genes, the microarray datasets GSE19429, GSE58831, and GSE2779 were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) in MDS were screened using RStudio, and overlapped DEGs were obtained with Venn Diagrams. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses, and protein–protein interaction network were performed. Quantitative real-time PCR (qRT-PCR) was employed to confirm the microarray results. This study identified 26 DEGs. Functional enrichment analyses indicated that these DEGs were significantly enriched in the immune response, and hematopoietic cell lineage. Eight core genes, for example, RAG1 and PAX5, were identified with a high degree of connectivity. The result of qRT-PCR showed that RAG1 was significantly down-regulated in MDS patients, which helped in distinguishing MDS patients from normal controls. The area under the curve of the receiver operator characteristic was 0.913 (P < 0.0001). MDS patients with low RAG1 expression level had a poor long-term survival (P = 0.031). What's more, the expression of RAG1 was significantly increased in the patients who received treatment. The results showed that the expression of RAG1 was down-regulated in MDS patients. Lower RAG1 expression was associated with adverse clinical outcomes. RAG1 may be a potential prognostic biomarker for MDS. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is a malignant clonal disease characterized by abnormal proliferation of immature myeloid cells and bone marrow failure. Regulatory T cells (Treg) play a suppressive role in the anti-tumor immune response in the tumor microenvironment. Screening biomarkers based on Treg immune-related genes may help to predict the prognosis and the efficacy of immunotherapy of AML. Gene expression profiles of AML (non-M3) were obtained from the TCGA and GEO databases. Gene module related to Treg was extracted using CIBERSORT and WGCNA algorithms. Univariate Cox regression and LASSO analyses were performed to identify hub genes and constructed the immune prognostic model. Molecular and immunological features associated with risk signature were explored, and TIDE was used to predict the efficacy of immunotherapy. A risk signature was constructed based on the five IRGs (IFI27L1, YIPF6, PARVB, TRIM32 and RHOBTB3). The risk signature could be served as an independent prognostic factor of AML. Patients in the high-risk group had a poorer OS than those in the low-risk group. In addition, patients in the high-risk group had higher TP53 mutation rate, higher infiltration of Treg, higher immune escape potential and less benefit from ICI therapy compared to low-risk group. Our study constructed a prognostic index based on five Treg-related biomarkers, which help to facilitate the differentiation of immunological and molecular characteristics of AML, predict patient prognosis and provide a reference for predicting benefits from ICI therapy. [ABSTRACT FROM AUTHOR]