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Objectives To investigate all pregnancies and analyze the factors influencing pregnancy outcomes in patients with adenomyosis after high intensity focused ultrasound (HIFU).Materials and methods A total of 231 patients with adenomyosis who completed HIFU and wished to conceive were enrolled. The symptom improvement and information of pregnancy were recorded during the follow-up period. Factors influencing pregnancy outcomes were analyzed using multivariate regression analysis and survival analysis.Results After HIFU, 100 of 231 (43.3%) patients became pregnant within 96 months, including 77 (77/194, 39.7%) in natural and 23 (23/37, 62.2%) in vitro fertilization and embryo transfer (IVF-ET) pregnancies following gonadotropin-releasing hormone agonist (GnRHa). Among the 108 (46.8%, 108/231) infertile patients (defined as the failure to achieve pregnancy after 12 months of regular unprotected sexual intercourse, 40 primary infertility and 68 secondary infertility), 31 (28.7%) became pregnant. At the end of the follow-up, 70 successfully delivered 71 healthy babies. No uterine rupture occurred during pregnancy and delivery. Patients with pelvic adhesion and infertility history had a lower pregnancy chance than that of patients without pelvic adhesion and infertility history (OR < 1, p

Abstract A positive correlation between wealth and biodiversity within cities is a commonly documented phenomenon in urban ecology that has come to be labeled as the “luxury effect.” We contend that both this language and this framing restrict our understanding of how sociopolitical power dynamics influence biodiversity within and across cities. We describe how the term “luxury” is not appropriately applied to describe patterns of biodiversity and how the pattern depends on the form(s) of biodiversity investigated. While we recognize examples where there is a positive relationship between socioeconomic status and biodiversity, we describe numerous examples where either opposite patterns or no clear relationship between wealth and biodiversity is found. We propose an alternate framework, the POSE framework, that examines the Power, Objectives, mediating Socio‐ecological context, and Effort of specific actors and how those may influence biodiversity. The mediating socio‐ecological context includes everything from biophysical limitations to historical context and the actions of other actors. Further, it is important to understand how and to what degree we expect the actor's actions to influence biodiversity in order to design studies that are able to detect these shifts in biodiversity. We contend that complicating our analysis to focus more on power generally, rather than socioeconomic status specifically, as well as the specific objectives of actors of interest within their socio‐ecological context offers a more flexible approach that can be applied in a wider range of socio‐ecological contexts and allows for more directed policy interventions.

Abstract Evolution of SARS-CoV-2 variants emphasizes the need for multivalent vaccines capable of simultaneously targeting multiple strains. SCTV01E is a tetravalent COVID-19 vaccine derived from the spike protein of SARS-CoV-2 variants Alpha, Beta, Delta, and Omicron BA.1. In this double-blinded placebo-controlled pivotal efficacy trial (NCT05308576), the primary endpoint was vaccine efficacy (VE) against COVID-19 seven days post-vaccination in individuals without recent infection. Other endpoints included evaluating safety, immunogenicity, and the VE against all SARS-CoV-2 infections in individuals meeting the study criteria. Between December 26, 2022, and January 15, 2023, 9,223 individuals were randomized at a 1:1 ratio to receive SCTV01E or a placebo. SCTV01E showed a VE of 69.4% (95% CI: 50.6, 81.0) 7 days post-vaccination, with 75 cases in the placebo group and 23 in the SCTV01E group for the primary endpoint. VEs were 79.7% (95% CI: 51.0, 91.6) and 82.4% (95% CI: 57.9, 92.6), respectively, for preventing symptomatic infection and all SARS-CoV-2 infections 14 days post-vaccination. SCTV01E elicited a 25.0-fold higher neutralizing antibody response against Omicron BA.5 28 days post-vaccination compared to placebo. Reactogenicity was generally mild and transient, with no reported vaccine-related SAE, adverse events of special interest (AESI), or deaths. The trial aligned with the shift from dominant variants BA.5 and BF.7 to XBB, suggesting SCTV01E as a potential vaccine alternative effective against present and future variants.

Abstract Hepatocellular carcinoma (HCC) is a highly heterogeneous and malignant cancer with poor overall survival. The application of sorafenib is a major breakthrough in the treatment of HCC. In our study, FOXQ1 was significantly overexpressed in sorafenib-resistant HCC cells and suppressed sorafenib-induced ferroptosis. We found that phosphorylation of FOXQ1 at serine 248 is critical for the suppression of sorafenib-induced ferroptosis. Furthermore, as the upstream phosphorylation kinase of FOXQ1, JNK1, which is activated by sorafenib, can directly phosphorylate the serine 248 site of FOXQ1. Then, the phosphorylated FOXQ1 got a high affinity for the promoter of ETHE1 and activates its transcription. Further flow cytometry results showed that ETHE1 reduced intracellular lipid peroxidation and iron levels. Collectively, our study implicated the JNK1-FOXQ1-ETHE1 axis in HCC ferroptosis induced by sorafenib, providing mechanistic insight into sensitivity to sorafenib therapy of HCC.

Abstract Colorectal cancer (CRC) remains a significant global health issue with high incidence and mortality. Yin Yang 1 (YY1) is a powerful transcription factor that acts dual roles in gene activation and repression. High expression level of YY1 has been reported in CRC, indicating the existence of stable factors of YY1 in CRC cells. We aimed to identify the key molecules and underlying mechanisms responsible for stabilizing YY1 expression in CRC. Mass spectrometry analysis was utilized to identify USP7 as a potential molecule that interacted with YY1. Mechanically, USP7 stabilizes YY1 expression at the protein level by interfering its K63 linkage ubiquitination. YY1 exerts its oncogenic function through transcriptionally activating TRIAP1 but suppressing LC3B. In addition, at the pathological level, there is a positive correlation between the expression of YY1 and the budding of CRC. This study has revealed the intricate interplay between YY1 and USP7 in CRC, suggesting that they could serve as novel therapeutic targets or predictive biomarkers for CRC patients.

Background and aims: Bone marrow failure (BMF) is chronic benzene-induced hematotoxicity, which is associated with differential gene expression abnormality. Benzene-induced BMF is characterized by irreversible bone marrow depression. Despite extensive studies have been conducted, there is a lack of reliable, useful and simple diagnostic method for BMF. Previous studies have shown that the aberrant gene expression changes and reactive oxygen species production in bone marrow cells related to the development of BMF. Early detection of differentially expressed genes (DEGs) as potential biomarkers is important for diagnosis and treatment. However, the validation of effective biomarker through DEGs analysis in benzene-induced BMF still deserve to be clarified. This study aimed to identify target genes as potential biomarkers with benzene-induced BMF based on DEGs analysis. Methods: First, we developed a benzene-induced BMF mouse model and obtained the DEGs in bone marrow cells of benzene-exposed CD1 mice. Next, after obtaining the DEGs via RNA-Sequencing (RNA-seq) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were also used, key genes associated with benzene-induced BMF were identified. Additionally, the key markers for benzene poisoning was evaluated using qRT-PCR technique. Results: We identified DEGs for further KEGG functional analysis. Ten statistically significantly (up or down) regulated genes, namely Mapk11, Foxo1, Lefty1, Ren1, Bank1, Fgf3, Cdc42ep2, Rasgrf1, P2rx7, and Shank3 were found mainly associated with mitogen-activated protein kinases (MAPK) oxidative stress pathway. Further analysis using qRT-PCR identified that eight statistically significant DEGs associated with signaling pathways such as MAPK. We found that the level of mRNA expression of Mapk11, Foxo1, Bank1, Lefty1, Ren1, P2rx7, and Fgf3 genes were increased and Cdc42ep2 gene was decreased in BMF mice compared to control mice. Additionally, we validated the eight candidate genes for potential biomarkers in peripheral blood mononuclear cells of benzene poisoning patients by qRT-PCR. Conclusion: Our results indicated that Mapk11 and Fgf3 were predominantly candidate genes linked to novel biomarkers for benzene hematotoxicity in human beings. Our study will provide new candidate genes as useful biomarkers involved in benzene-induced hematotoxicity.

Abstract Glioblastoma (GBM) is the most common malignant primary brain tumor. Despite comprehensive treatment with traditional surgery, radiotherapy, and chemotherapy, the median survival rate is

Abstract The metastasis of non-small cell lung cancer (NSCLC) is the leading death cause of NSCLC patients, which requires new biomarkers for precise diagnosis and treatment. Circular RNAs (circRNAs), the novel noncoding RNA, participate in the progression of various cancers as microRNA or protein sponges. We revealed the mechanism by which circEPB41L2 (hsa_circ_0077837) blocks the aerobic glycolysis, progression and metastasis of NSCLC through modulating protein metabolism of PTBP1 by the E3 ubiquitin ligase TRIP12. With ribosomal RNA-depleted RNA seq, 57 upregulated and 327 downregulated circRNAs were identified in LUAD tissues. circEPB41L2 was selected due to its dramatically reduced levels in NSCLC tissues and NSCLC cells. Interestingly, circEPB41L2 blocked glucose uptake, lactate production, NSCLC cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, acting as a scaffold, circEPB41L2 bound to the RRM1 domain of the PTBP1 and the E3 ubiquitin ligase TRIP12 to promote TRIP12-mediated PTBP1 polyubiquitylation and degradation, which could be reversed by the HECT domain mutation of TRIP12 and circEPB41L2 depletion. As a result, circEPB41L2-induced PTBP1 inhibition led to PTBP1-induced PKM2 and Vimentin activation but PKM1 and E-cadherin inactivation. These findings highlight the circEPB41L2-dependent mechanism that modulates the “Warburg Effect” and EMT to inhibit NSCLC development and metastasis, offering an inhibitory target for NSCLC treatment.

Abstract Many types of cancer cells, including colorectal cancer cells (CRC), can simultaneously enhance glycolysis and repress the mitochondrial tricarboxylic acid (TCA) cycle, which is called the Warburg effect. However, the detailed mechanisms of abnormal activation of the glycolysis pathway in colorectal cancer are largely unknown. In this study, we reveal that the protein arginine methyltransferase 1 (PRMT1) promotes glycolysis, proliferation, and tumorigenesis in CRC cells. Mechanistically, PRMT1-mediated arginine asymmetric dimethylation modification of phosphoglycerate kinase 1 (PGK1, the first ATP-producing enzyme in glycolysis) at R206 (meR206-PGK1) enhances the phosphorylation level of PGK1 at S203 (pS203-PGK1), which inhibits mitochondrial function and promotes glycolysis. We found that PRMT1 and meR206-PGK1 expression were positively correlated with pS203-PGK1 expression in tissues from colorectal cancer patients. Furthermore, we also confirmed that meR206-PGK1 expression is positively correlated with the poor survival of patients with colorectal cancer. Our findings show that PRMT1 and meR206-PGK1 may become promising predictive biomarkers for the prognosis of patients with CRC and that arginine methyltransferase inhibitors have great potential in colorectal cancer treatment.

Transformer oil plays the role of heat dissipation and insulation in power transformers, and its electrical and thermal characteristics are directly related to the stable operation of the transformer. At the same time, it is important to master the electric–thermal characteristics of transformer oil for transformer state evaluation, latent fault prediction, and maintenance planning. Based on this, the gas production rule and electrical characteristics of transformer oil under accelerated aging are studied in this paper. First, the experimental platform for power transformer aging is established to accelerate the aging of power transformers. Second, the accelerated aging transformer oil is taken as the research object, and the power frequency, DC, lightning, and gas chromatography are measured and analyzed. Finally, a transformer oil aging evaluation model is established, which takes into account four factors: carbon and oxygen gas factors in transformers, life loss factors calculated by hotspot temperature, hydrocarbon gas factors dissolved in transformer oil, and oil quality factors, and conducts aging evaluation. The conclusion shows that the T parameter proposed in this paper can effectively evaluate the quality of transformer oil. When T is less than or equal to 0.6, there is no aging of the oil. When T is greater than 0.6 and less than 1, the transformer oil has been aging, but it is not manifested. Those are parameters whose chromatography and breakdown voltage are not far beyond the IEEE standard. When T = 1, the aging of oil with significant changes in gas content and breakdown voltage can be observed. When T is greater than 1, the oil has undergone serious aging.

To alleviate bone loss, most current drugs target osteoclasts. Saikosaponin A (Ssa), a triterpene saponin derived from Bupleurum falcatum (also known as Radix bupleuri), has immunoregulatory, neuromodulatory, antiviral, anticancer, anti-convulsant, anti-inflammatory, and anti-proliferative effects. Recently, modulation of bone homeostasis was shown to involve ferroptosis. Herein, we aimed to determine Ssa’s inhibitory effects on osteoclastogenesis and differentiation, whether ferroptosis is involved, and the underlying mechanisms. Tartrate‐resistant acid phosphatase (TRAP) staining, F‐actin staining, and pit formation assays were conducted to confirm Ssa-mediated inhibition of RANKL-induced osteoclastogenesis in vitro. Ssa could promote osteoclast ferroptosis and increase mitochondrial damage by promoting lipid peroxidation, as measured by iron quantification, FerroOrange staining, Dichloro-dihydro-fluorescein diacetate, MitoSOX, malondialdehyde, glutathione, and boron-dipyrromethene 581/591 C11 assays. Pathway analysis showed that Ssa can promote osteoclasts ferroptosis by inhibiting the Nrf2/SCL7A11/GPX4 axis. Notably, we found that the ferroptosis inhibitor ferrostatin-1 and the Nrf2 activator tert-Butylhydroquinone reversed the inhibitory effects of Ssa on RANKL-induced osteoclastogenesis. In vivo, micro-computed tomography, hematoxylin and eosin staining, TRAP staining, enzyme-linked immunosorbent assays, and immunofluorescence confirmed that in rats with periodontitis induced by lipopolysaccharide, treatment with Ssa reduced alveolar bone resorption dose-dependently. The results suggested Ssa as a promising drug to treat osteolytic diseases.

Aims: Cellular dormancy is a state of quiescence subpopulation of tumor cells, characterized by low differentiation and lack of mitotic activity. They could evade chemotherapy and targeted therapy, leading to drug resistance and disease recurrence. Recent studies have shown a correlation between dormant cancer cells and unique extracellular matrix (ECM) composition, which is critical in regulating cell behavior. However, their interacting roles in TNBC patients remains to be characterized. Main methods: Dormant cancer cells in MDA-MB-231 cell line with highest PKH26 dye-retaining were FACS-sorted and gene expression was then analyzed. Dormant associated ECM (DA-ECM) signature was characterized by pathway analysis. Unsupervised hierarchical clustering was used to define distinct ECM features for TNBC patients. ECM-specific tumor biology was defined by integration of bulk RNA-seq with single-cell RNA-seq data, analysis of ligand-receptor interactions and enriched biological pathways, and in silico drug screening. We validated the sensitivity of dormant cancer cells to MAPK inhibitors by flow cytometry in vitro. Key findings: We observed that dormant TNBC cells preferentially expressed ∼10 % DA-ECM genes. The DA-ECM High subtype defined by unsupervised hierarchical clustering analysis was associated with immunosuppressive tumor microenvironment. Moreover, ligand-receptor interaction and pathway analysis revealed that the DA-ECM High subtype may likely help maintain tumor cell dormancy through MAPK, Hedgehog and Notch signaling pathways. Finally, in silico drug screening against the DA-ECM signature and in vitro assay showed dormant cancer cells were relatively sensitive to the MAPK pathway inhibitors, which may represent a potential therapeutic strategy for treating TNBC. Significance: Collectively, our research revealed that dormancy-associated ECM characterized tumor cells possess significant ECM remodeling capacity, and treatment strategies towards these cells could improve TNBC patient outcome.

This article introduces a novel petal-like SAW topology insulator, which can transmit sound waves with low loss and high flexibility in an ultra-wide frequency band by simultaneously adjusting multiple structural parameters of phononic crystals. Using finite element analysis, it was found that adjusting these parameters can generate a broadband gap of 55.8–65.7 MHz. This structure can also achieve defect immunity and sharp bending in waveguide transmission. When this topology insulator is applied to resonators, compared to traditional designs, the insertion loss is reduced by 22 dB, the on-load quality factor is increased by 227%, the off-load quality factor is increased by 1024.5%, and the quality sensitivity is improved by 3.7 times compared to bare devices.

Since a multiaxial loading environment may lead to the fatigue failure of structures, establishing a reliable fatigue model to predict the multiaxial fatigue lives of structures has always been a concern of engineers. This study proposes a new multiaxial fatigue theoretical model (WYT model) based on the critical plane theory, which takes the plane of the maximum shear strain amplitude as the critical plane and considers the effects of shear stress and normal stress on fatigue damage. Moreover, a backpropagation neural network (BPNN) model for multiaxial fatigue life prediction with the shear strain amplitude, normal strain amplitude, mean shear stress, and mean normal stress on the same critical plane as input parameters and fatigue life as the output variable is established. Finally, the WYT model and the BPNN model are compared with two existing multiaxial fatigue models to evaluate the life prediction effects of different models for S45C and 7075-T651 under constant-amplitude and variable-amplitude multiaxial loadings. The calculation results show that the WYT model is feasible, and the BPNN model is more accurate in predicting the fatigue lives of specimens than other multiaxial fatigue theoretical models.

The converter transformer is an electrical equipment with a symmetrical structure. Due to its symmetry, the ground current should be small when the core is grounded at one point. The research and analysis of grounding currents in the converter transformer can effectively help staff to judge the working state of the converter transformer. Therefore, it is very meaningful to study the calculation problem of the grounding current under the multi-point grounding state. First of all, a homogenization modeling method considering the characteristics material of the core silicon steel sheet is proposed; secondly, on this basis, the finite element simulation model of multi-point grounding of the core of the converter transformer is established and simulated; then a multi-point grounding test was conducted using the shrinkage model of the converter transformer to verify the finite element simulation results; the final consequence show that the homogenization modeling method can effectively calculate the grounding current at multi-grounding.

The minerals in coal are transformed to the coal slag during the entrained-flow coal gasification process. The stable operation of the gasifier relies on the smooth slag tapping process. The flow behavior of coal slag is quantified by the viscosity. The high-iron coal (w(Fe2O3)>15%, ash basis) is widely distributed in China. The iron (Fe2+ or Fe3+) in the coal slag is easily transformed to the metallic iron due to the high content of the reducing gas in the Shell coal gasifier. The presence of metallic iron may lead to the slag blockage or even the unscheduled shut-down of coal gasifier. Hence, it is necessary to investigate the metallic iron precipitation behavior and its effect on coal slag viscosity. The precipitation behavior of metallic iron is investigated by the thermodynamic modelling. Then, the kinetic models of the metallic iron precipitation and agglomeration are built, respectively. Finally, the effects of metallic iron on the crystallization and viscosity of coal slag are quantified. The metallic iron is precipitated under the Shell coal gasifier atmosphere. The high-CaO coal slag favors the metallic iron formation. The metallic iron precipitation model is built based on the diffusion behavior of the reducing gas in the coal slag. In contrast, the metallic iron agglomeration model is established according to the sedimentation of metallic iron particles in the liquid coal slag. Both increasing the CaO content of coal slag and employing high slagging temperature results in the drop of slag viscosity, and the low slag viscosity improves the iron reduction process and metallic iron sedimentation. Therefore, the precipitation and agglomeration of metallic iron are improved. The critical time (tc) of metallic iron agglomeration is proposed and is used as the guide to prevent the metallic iron agglomeration. The metallic iron agglomeration can be alleviated by decreasing the slag tapping temperature or reducing the CaO content of coal slag. The traditional KJMA model is modified by considering the thermodynamic equilibrium content of solid phase in the slag. The metallic iron induces the strong crystallization of anorthite in slag and the slag viscosity is therefore significantly increased. The time of slag viscosity increasing to 25 Pa·s is decreased with the slag tapping temperature, while the time of the solid content achieving the thermodynamic equilibrium is increased. The study demonstrates that the metallic iron precipitation and agglomeration can be alleviated by adopting a low slag tapping temperature, or by using the silicon-rich additive, or co-gasifying with the high-silicon coal during the entrained-flow gasification of high-iron coal.

Radiation therapy is a primary treatment for hepatocellular carcinoma (HCC), but its effectiveness can be diminished by various factors. The over-expression of PD-L1 has been identified as a critical reason for radiotherapy resistance. Previous studies have demonstrated that nifuroxazide exerts antitumor activity by damaging the Stat3 pathway, but its efficacy against PD-L1 has remained unclear. In this study, we investigated whether nifuroxazide could enhance the efficacy of radiotherapy in HCC by reducing PD-L1 expression. Our results showed that nifuroxazide significantly increased the sensitivity of tumor cells to radiation therapy by inhibiting cell proliferation and migration while increasing apoptosis in vitro. Additionally, nifuroxazide attenuated the up-regulation of PD-L1 expression induced by irradiation, which may be associated with increased degradation of PD-L1 through the ubiquitination-proteasome pathway. Furthermore, nifuroxazide greatly enhanced the efficacy of radiation therapy in H22-bearing mice by inhibiting tumor growth, improving survival, boosting the activation of T lymphocytes, and decelerating the ratios of Treg cells in spleens. Importantly, nifuroxazide limited the increased expression of PD-L1 in tumor tissues induced by radiation therapy. This study confirms, for the first time, that nifuroxazide can augment PD-L1 degradation to improve the efficacy of radiation therapy in HCC-bearing mice.

For the detections of typical faults gases, namely NO2 and O3, in the air insulated switchgears (AIS), we purpose Au- and B-embedded graphene (Au- and B-graphene) as promising sensing material using the first-principles theory. We firstly investigate the Au- and B-embedding behavior on the graphene, and find that both Au and B atoms are chemical stably adsorbed on the vacancy-defected graphene; in the gas adsorbed systems, it is found that NO2 and O3 adsorptions on Au-graphene are identified as chemisorption, while those on B-graphene are physisorption. The electronic properties of Au- and B-graphene in the gas adsorptions indicate the resistance-type sensing potential of Au-graphene upon O3 as well as that of B-graphene upon NO2. Besides, Au-graphene is a promising WF-based gas sensor upon NO2 and O3. The findings in this work uncover the strong potentials of Au- and B-graphene for detections of the NO2 and O3 in AIS, which gives the guidance to explore novel graphene-based gas sensors for applications in the power system.

Summary: Polypyrimidine tract-binding protein 3 (PTBP3) plays an important role in the post-transcriptional regulation of gene expression, including mRNA splicing, translation, and stability. Increasing evidence has shown that PTBP3 promotes cancer progression in several tumor types. However, the molecular mechanisms of PTBP3 in renal cell carcinoma (RCC) remain unknown. Here, tissue microarrays (TMAs) suggested that PTBP3 expression was increased in human RCC and that high PTBP3 expression was correlated with poor five-year overall survival and disease-free survival. We also showed that PTBP3 binds with HMGA1 mRNA in the 3′UTR region and let-7 miRNAs. PTBP3 interacted with IGF2BP3, and the PTBP3/IGF2BP3 axis prevented let-7 mediated HMGA1 mRNA silencing. PTBP3 promotes renal cancer cell growth and metastasis in vitro and in vivo. Taken together, our findings indicate PTBP3 serves as a regulator of HMGA1 and suggest its potential as a therapeutic agent for RCC.

Abstract Background Yin Yang‐1 (YY1) is identified as a transcription factor with multiple functions. However, the role of YY1 in tumorigenesis remains controversial and its regulatory effects may depend upon not only cancer types, but also its interacting partners, chromatin structure, and the context in which it acts. It has been detected that YY1 was highly expressed in colorectal cancer (CRC). Intriguingly, many YY1‐repressed genes exhibit tumor suppressive potential while YY1 silencing is related to chemotherapy resistance. Therefore, it is crucial to meticulously explore YY1 protein structure and the dynamic alteration of its interactome in each cancer type. This review attempts to describe the structure of YY1, summarize the mechanism that influence the expression level of YY1 and also highlight the recent advances in our understanding of regulatory insights of YY1 functions in CRC. Methods Related studies were identified through scoping search of PubMed, Web of science, Scopus and Emhase concerning the terms of “colorectal cancer”, colorectal carcinoma” or CRC with “YY1”. The retrieval strategy included title, abstract, and keywords with no language limitations. All the included articles were categorized depending on the mechanisms they explored. Results In total, 170 articles were identified for further screening. After removing the duplication, not relevant outcomes and review articles, 34 were finally included in the review. Among them, 10 articles revealed the reasons of YY1 high expression in CRC, 13 articles explored YY1 function in CRC, and 11 articles fell into both aspects. In addition, we also summarized 10 clinical trials concerning the expression and activity of YY1 in various diseases, which offers a hint for future application. Conclusions YY1 is highly expressed in CRC and broadly recognized as an oncogenic factor during the whole course of CRC. Sporadic controversial views are raised in term of CRC treatment, reminding us that future studies should take the influence of therapeutic regimens into concern.

Abstract Protein arginine methyltransferase 2 (PRMT2) is involved in several biological processes via histone methylation and transcriptional regulation. Although PRMT2 has been reported to affect breast cancer and glioblastoma progression, its role in renal cell cancer (RCC) remains unclear. Here, we found that PRMT2 was upregulated in primary RCC and RCC cell lines. We demonstrated that PRMT2 overexpression promoted RCC cell proliferation and motility both in vitro and in vivo. Moreover, we revealed that PRMT2-mediated H3R8 asymmetric dimethylation (H3R8me2a) was enriched in the WNT5A promoter region and enhanced WNT5A transcriptional expression, leading to activation of Wnt signaling and malignant progression of RCC. Finally, we confirmed that high PRMT2 and WNT5A expression was strongly correlated with poor clinicopathological characteristics and poor overall survival in RCC patient tissues. Our findings indicate that PRMT2 and WNT5A may be promising predictive diagnostic biomarkers for RCC metastasis. Our study also suggests that PRMT2 is a novel therapeutic target in patients with RCC.

With the gradual emphasis on health by people, the research on the pathogenesis of endemic diseases has become increasingly in-depth. Through analyzing the environmental selenium characteristics and conducting a comparative study in typical areas of Chinese loess and black soil in this paper, it is concluded that the environmental selenium in the two regions has different characteristics. The soil in the loess area has the characteristics of high alkalinity, low selenium, and relatively high selenium availability, and the crops are selenium-deficient, while the soil in the black soil area has the characteristics of high organic matter, low selenium availability, and relatively high selenium in crops. The research concluded that the environmental occurrence mechanism of Keshan disease in the loess area and the black soil area is different. Keshan disease can be induced in both low-selenium and sufficient-selenium environments, and environmental selenium should be one of the inducing factors of Keshan disease. This research provides a reference for predicting the areas where Keshan disease occurs and for disease prevention, and it can also serve in the prevention and control of endemic diseases.

BackgroundAcute respiratory distress syndrome (ARDS) / acute lung injury (ALI) is a serious medical disease characterized by pulmonary dysfunction and inflammation. This study aims to determine the main molecular modules linked to ARDS and investigate the role of Fibulin-1 (FBLN1) in regulating ferroptosis in ARDS.MethodsWeighted Gene Co-expression Network Analysis (WGCNA) was employed on the GSE263867 dataset to find key modules associated with ALI. Differentially expressed genes (DEGs) and protein-protein interaction (PPI) networks were analyzed. MLE-12 cells were treated with lipopolysaccharide (LPS) to induce ferroptosis. In vitro studies were conducted to investigate the effects of FBLN1 and Transforming Growth Factor Beta 1 (TGF-β) overexpression on cell viability, oxidative stress markers, and ferroptosis-related proteins.ResultsWGCNA identified the turquoise module as significantly negatively correlated with ARDS. Five key overlapping genes (GRIA1, OGN, COL14A1, FBLN1, and COL6A3) were significantly downregulated in ARDS samples. LPS treatment induced ferroptosis in MLE-12 cells, indicated by increased malondialdehyde (MDA), lipid reactive oxygen species (ROS), and ferrous iron (Fe2⁺) levels, and decreased cell viability and glutathione (GSH) levels. FBLN1 overexpression partially reversed these effects. Additionally, FBLN1 inhibited the TGF-β/Smad signaling pathway, as shown by decreased TGF-β and p-Smad protein levels. TGF-β overexpression exacerbated LPS-induced oxidative stress and ferroptosis, reducing cell viability and GSH levels. FBLN1 overexpression counteracted this effect, suggesting antagonistic roles for FBLN1 and TGF-β in regulating ferroptosis.ConclusionThis study highlights FBLN1 as a critical regulator of ferroptosis in ARDS. Targeting the TGF-β/Smad pathway to modulate FBLN1 expression offers a potential therapeutic strategy to alleviate oxidative stress and mitigate pulmonary injury in inflammatory lung diseases.

Phosphorus, particularly the red phosphorus (RP) allotrope, has been extensively studied as an anode material in both lithium-ion batteries (LIBs) and emerging sodium-ion batteries (SIBs). RP is featured with high theoretical capacity (2,596 mA h g−1), suitable low redox potential (~0.7/0.4 V for LIBs/SIBs), abundant resources, and environmental friendliness. Despite its promises, the inherent poor electrical conductivity of RP (~10−14 S cm−1) and significant volume changes during charge/discharge processes (>300%) compromise its cycling stability. In order to address these issues, various countermeasures have been proposed, focusing on the incorporation of materials that provide high conductivity and mechanical strength in composite-type anodes. In addition, the interfacial instability, oxidation, and safety concerns and the low mass ratio of active material in the electrode need to be addressed. Herein, this review summarizes the up-to-date development in RP materials, outlines the challenges, and presents corresponding countermeasures aimed to enhance the electrochemical performance. It covers aspects such as the structural design of RP, the choice of the additive materials and electrolytes, rational electrode construction, etc. The review also discusses the future prospects of RP for LIBs/SIBs and aims to provide a different perspective on the challenges that must be overcome to fully exploit the potential of RP and meet commercial application requirements.

When the converter transformer core is grounded at multi-points, a fault loop will be formed and a circulation will be generated, leading to local overheating of the magnetic core and decomposition of insulating oil. Therefore, the converter transformer core will be single point grounded. As a rare internal lead of converter transformer, the ground current on the core ground lead can often reflect the running state of converter transformer. In this paper, theoretical analysis, modeling simulation and experimental research are carried out on the ground current of converter transformer at one point. Firstly, according to the structure characteristics of converter transformer, the analytical modeling of ground current is carried out. Secondly, based on the structure characteristics of oil paper insulation, the equivalent capacitance of converter transformer is calculated. Then, the analytical and finite element simulation model of converter transformer is established, and the ground current of converter transformer is calculated. Finally, the correctness of the proposed scheme is verified by measuring the grounding current of converter transformer core.

PURPOSETo study sacral injuries and influencing factors after ultrasonic ablation of uterine fibroids no more than 30 mm from the sacrum.METHODSA total of 406 patients with uterine fibroids who underwent percutaneous ultrasound ablation were analyzed retrospectively. All patients underwent contrast-enhanced magnetic resonance imaging (MRI) scans before and after high-intensity focused ultrasound. The abnormal signal intensity (low signal intensity on T1WI and high signal intensity on T2WI) on the postoperative MRIs was indicative of a sacral injury. The patients were divided into a sacrum injury group and a sacrum non-injury group. The relationship between fibroid characteristics, ultrasound ablation parameters, and injury was analyzed using univariate and multivariate analyses.RESULTSThere were 139 cases of sacral injury (34.24%). When the distance from the fibroid’s dorsal side to the sacrum was 0–10 mm, the risk assessment showed that the danger of sacral injury increased by 1.85 times and 3.03 times compared with that at a distance of 11–20 or 21–30 mm. Furthermore, the risk of sacral injury increased by 1.89 times and 3.23 times when the therapeutic dose (TD) of a fibroid was >500 KJ compared with that of a fibroid with TD= 250–500 KJ and 500 KJ were significantly correlated with sacral injury. The distance from the fibroid’s dorsal side to the sacrum and the TD were the main causes of injury to the sacrum. A distance of 10 mm or less and a TD of >500 KJ carried higher injury risks, while a distance of 21–30 mm and a TD of

Abstract Background Metabolic reprogramming is a hallmark of various cancers. Targeting metabolic processes is a very attractive treatment for cancer. Renal cell carcinoma (RCC) is a type of metabolic disease, and the lipidomic profile of RCC is significantly altered compared with that of healthy tissue. However, the molecular mechanism underlying lipid metabolism regulation in RCC is not clear. Methods The XF long-chain fatty acid oxidative stress test kits were used to assess the dependence on long-chain fatty acids and mitochondrial function after knockdown TRIM21 in RCC cells. The effect of TRIM21 on the lipid content in RCC cells was determined by metabolomics analysis, Oil Red O staining, and cellular Nile red staining. qRT-PCR and western blot were used to explore the relationship between TRIM21 and lipogenesis, and then the key molecule sterol regulatory element binding transcription factor 1 (SREBF1) was identified to interact with TRIM21 by immunoprecipitation, which was also identified in an orthotopic model. Subsequently, the relevance and clinical significance of TRIM21 and SREBF1 were analyzed by The Cancer Genome Atlas (TCGA) database, and 239 tissues were collected from RCC patients. Results TRIM21 silencing attenuated the dependence of RCC cells on fatty acids, and enhanced lipid accumulation in RCC cells. TRIM21 overexpression significantly decreased lipid contents by decreasing the expression of lipogenic enzymes via ubiquitination-mediated degradation of SREBF1. SREBF1 is critical for TRIM21-mediated lipogenesis inhibition in vitro and in vivo. Moreover, TRIM21 expression is negatively correlated with SREBF1 expression, and TRIM21-SREBF1 is a reliable combinational biomarker for RCC prognosis. Conclusion The findings from this study reveal a novel pathway through which TRIM21 inhibits the lipid metabolism process of RCC and shed light on the development of targeted metabolic treatment and prognosis diagnosis of RCC.

Objective To investigate the value of the image indexes of B-mode and power Doppler sonography in predicting the therapeutic efficacy of high intensity focused ultrasound (HIFU) ablation for uterine fibroids.Materials and methods Two hundred and three patients with a solitary uterine fibroid were enrolled in this study. Every patient underwent transvaginal sonography (TVS) and magnetic resonance imaging (MRI) before HIFU. The patients were divided into hypointense, isointense and hyperintense fibroid groups based on T2 weighted MR imaging characteristics, and ultrasonic image indexes of the fibroids in different groups were compared. Multiple linear regression analysis was used to evaluate the correlation between ultrasonic image indexes and energy efficiency factor (EEF), non-perfused volume (NPV) ratio of uterine fibroids.Results Among them, 72 patients had a hypointense fibroid, 70 had an isointense fibroid and 61 had a hyperintense fibroid. Significant differences were observed in the ultrasound imaging gray scale value difference between the myometrium and uterine fibroids (GSmyo-fib), the ultrasound imaging gray scale value ratio of fibroids over the myometrium (GSfib/myo), and the ratio of power Doppler pixel area to fibroid area (PDPA/FA) among the three groups (p

Aims To evaluate the long-term survival benefits of high intensity focused ultrasound (HIFU) ablation in patients with hepatocellular carcinoma (HCC) combined with portal vein tumor thrombus (PVTT).Methods The data of patients with HCC-PVTT treated with HIFU from January 2014 to December 2019 were retrospectively analyzed. All patients received HIFU ablation for both PVTT and liver tumor in one session. Perioperative adverse events (AEs) were recorded, and follow-up was performed postoperatively. The Kaplan–Meier method was used for survival analysis.Results Median follow-up was 13.75 ± 1.31 months. A total of 144 patients (male/female: 122/22, age: 54.15 ± 11.84 years old) were included in the study. A total of 267 liver tumors (tumor number: 1.87 ± 1.65, range 1–10) were treated with HIFU. The mean ± SD diameter of viable liver tumors was 100.98 ± 61.65 mm. The reported postoperative AEs of HIFU were skin edema (93.75%), local pain (69.44%) and fever (7.64%). There was no liver failure, gastrointestinal bleeding or perioperative death. The median overall survival (OS) time was 14 months, while the cumulative survival rates of 0.5, 1, 2 and 3 years were 79.0%, 58.6%, 33.3% and 5.9%, respectively. The median OS of PVTT types I, II and III was 22, 13 and 14 months, respectively, and the difference was not statistically significant (p > 0.05).Conclusion HIFU is a minimally invasive method for HCC-PVTT with fewer complications, which could prolong the OS. Patients with PVTT type III could benefit more from HIFU, compared to types I and II.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease. Peripheral blood mononuclear cells (PBMCs) are any peripheral blood cell with round nuclei, including lymphocytes (T cells, B cells) and monocytes, whose physicochemical properties are randomized by obvious immune changes, and are a potentially effective source of SLE blood test samples and therapeutic targets. This study aimed to explore the upregulation molecules of PBMCs in patients with SLE and to explore their biological role. Homologous to the E6-AP carboxyl terminus (HECT) and regulator of chromosome condensation 1 (RCC1)-like domain (RLD) containing E3 ubiquitin protein ligase family member 6 (HERC6) expression was found significantly upregulated in four Gene Expression Omnibus gene sets. Moreover, HERC6 expression was upregulated in PBMCs from SLE patients compared with that in PBMCs from normal donors. HERC6 was significantly associated with SLE clinical phenotypes such as complement C3 content, erythrocyte sedimentation rate, and SLE disease activity index. In vitro, knockdown of HERC6 inhibited PBMC apoptosis, inflammatory response, and janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling pathway, while overexpression of HERC6 led to the opposite results. In addition, AG490, a JAK/STAT pathway inhibitor, reversed the promoting effect of HERC6 overexpression on PBMC apoptosis and inflammation. In conclusion, the level of HERC6 in PBMCs in patients with SLE was upregulated. Overexpression of HERC6 promoted PBMC apoptosis and inflammatory response, which was involved in the JAK/STAT pathway.

Modular multilevel converter (MMC) topology has received widespread attention in flexible DC transmission, power quality control, and other fields because of its high modularity and malleability characteristics, and has become one of the most promising topologies. However, owing to the characteristics of the MMC itself, the fluctuation of the capacitor voltage of the MMC sub-module is inversely proportional to the MMC working frequency. One of the main technical challenges for MMC is effectively suppressing the fluctuation of the capacitor voltage of the MMC sub-module when working at low frequencies. This study first analyzes the reasons for the fluctuation of the MMC sub-module capacitor voltage at low frequency. Then, based on the results of this analysis, we propose a suppression control strategy for the capacitor voltage fluctuation of the MMC sub-module in variable-frequency working situations. Finally, an MMC module was built using the MATLAB/Simulink environment for simulation verification, and a five-level MMC physical experimental platform was built for experimental verification. The simulation and experimental results demonstrate that the proposed suppression control strategy for the MMC sub-module capacitor voltage effectively suppresses the fluctuation of the capacitor voltage under variable-frequency working situations.

ABSTRACT Gut microbiota and their secreted metabolites have an influence on the initiation and progression of colon cancer. Probiotics are extensively perceived as a potential microbiota-modulation strategy to promote the health of the host, while the effectiveness of preventing colon cancer based on microbiota therapy has not been confirmed, and antitumor mechanisms influenced by microbiota and their metabolites with the intervention of probiotics remain to be further investigated. In vitro, Lactobacillus (JY300-8 and JMR-01) significantly inhibited the proliferation of CT26, HT29, and HCT116 cells. Moreover, we studied the prevention and therapy efficiency of Lactobacillus and its underlying antitumor mechanism through the alteration of gut microbiota and their metabolites regulated by Lactobacillus in colon cancer models in mice. We demonstrated that the pre-administration of Lactobacillus (JY300-8 and JMR-01) for 20 days before establishing tumor models resulted in an 86.21% reduction in tumor formation rate compared to tumor control group. Subsequently, continuous oral administration of living Lactobacillus significantly suppresses tumor growth, and tumor volumes decrease by 65.2%. Microbiome and metabolome analyses reveal that Lactobacillus suppresses colonic tumorigenesis and progression through the modulation of gut microbiota homeostasis and metabolites, including the down-regulation of secondary bile acids, sphingosine 1-phosphate (S1P), and pyrimidine metabolism, as well as the production of anticarcinogenic compounds in tumor-bearing mice. Additionally, metabolome analyses of Lactobacillus (JY300-8 and JMR-01) indicate that living Lactobacillus could reduce the relative abundance of alanine and L-serine to suppress tumor progression by regulating the tumor microenvironment, including down-regulation of pyrimidine metabolism and S1P signaling in cancer. These findings provide a potential prevention strategy and therapeutic target for colon cancer through the intervention of dietary Lactobacillus. IMPORTANCE The modulation of gut microbiota and metabolites has a significant influence on the progression of colon cancer. Our research indicated that the intervention of probiotics is a potentially feasible strategy for preventing colon cancer. We have also revealed the underlying antitumor mechanism through the alteration of gut microbiota and their metabolites, which could lead to broader biomedical impacts on the prevention and therapy of colon cancer with microbiota-based therapy regulated by probiotics.

In this paper, a novel single-phase double-leaf multi-stage acoustic black hole (SDM-ABH) is proposed. Compared with the traditional double-leaf ABH metamaterials, the unit cell consists of multiple sub-ABH structures arranged in a gradient periodically along the length direction. The energy band structure of the SDM-ABH metamaterial is calculated by the finite element method, and it is found that its weight decreases with the increase in the number of stages, but the bandgap ratio and attenuation both increase. By analysing the vibration modes at special points and the vibration displacement response of finite construction, it is revealed that strong attenuation at a low-frequency broadband is caused by the increase in the number of sub-ABHs that appear to have ABH effects due to the increase in the number of stages. In addition, the effect of structural parameters on the bandgap is investigated, and it is found that SDM-ABH metamaterials can be modulated at low frequencies by changing the truncation thickness and the power exponent of the sub-acoustic black hole, in which the increase in the truncation thickness t leads to the gradual weakening of the ABH effect of the sub-ABH until it disappears. The strong low-frequency attenuation properties of SDM-ABH metamaterials provide a method for a lightweight vibration damping design of metamaterials.

Converter transformer is the key equipment in UHVDC transmission. If a local overheating fault occurs, it will inevitably form a local hot spot on the core, winding or other structural parts. Among these faults, multipoint grounding and interlaminar short circuit faults account for 30–50% of core accidents. The continuous overheating of 150–250 °C will cause ablation on the silicon steel sheet, which will destroy the insulation material and reduce the insulation performance. In severe cases, it will cause thermal expansion, resulting in local deformation or displacement of the core. Considering the scale of size and temperature parameters, the scale model of converter transformer is established based on the principle of constant magnetic flux density. By using the homogenization theory, the scaled model under multipoint grounding and interlaminar short circuit fault is simulated by electromagnetic heat. First, the single-phase four-column model of the core is established according to the scaled principle, and the core is refined. Secondly, taking the refined model as the research object, the magnetic thermal coupling simulation and analysis are carried out under multi-point grounding and interlaminar short circuit fault, and the magnetic density, eddy current loss and temperature distribution on each lamination are obtained. Finally, the correctness of the simulation is verified by the one-dimensional eddy current loss analytical equation, which provides a reference for the local overheating problem of converter transformers.

Abstract Background DNMT1 has been shown to be highly expressed in a variety of cancers, including breast cancer. However, the mechanism is not very clear. Therefore, we aim to reveal the mechanism of DNMT1 highly express in breast cancer. And we also want to explore the role of DNMT1 in tumour microenvironment promoting breast cancer progression. Results In this study, we demonstrate that DNMT1 is overexpressed in breast cancer and that DNMT1 promotes breast cancer tumorigenesis and metastasis. We discovered that ZEB1 activates DNMT1 expression in breast cancer cells by recruiting P300 binding to the DNMT1 promoter and increasing its acetylation. Moreover, we revealed that tumour-associated macrophages (TAMs) increase DNMT1 expression in breast cancer cells via the IL-6-pSTAT3-ZEB1-DNMT1 axis in the tumour microenvironment. DNMT1 is required for TAM-mediated breast cancer cell migration. In addition, we confirmed that there were positive correlations among CD163 (TAM marker) expression, ZEB1 expression and DNMT1 expression in breast cancer patient tissues. Conclusions Our study indicates that DNMT1 is necessary for TAM-mediated breast cancer metastasis. Decitabine (DAC), as a specific DNA methylation inhibitor and FDA-approved drug, is a bona fide drug for breast cancer treatment.

Rapid progress in nanotechnology has advanced fundamental neuroscience and innovative treatment using combined diagnostic and therapeutic applications. The atomic scale tunability of nanomaterials, which can interact with biological systems, has attracted interest in emerging multidisciplinary fields. Graphene, a two-dimensional nanocarbon, has gained increasing attention in neuroscience due to its unique honeycomb structure and functional properties. Hydrophobic planar sheets of graphene can be effectively loaded with aromatic molecules to produce a defect-free and stable dispersion. The optical and thermal properties of graphene make it suitable for biosensing and bioimaging applications. In addition, graphene and its derivatives functionalized with tailored bioactive molecules can cross the blood–brain barrier for drug delivery, substantially improving their biological property. Therefore, graphene-based materials have promising potential for possible application in neuroscience. Herein, we aimed to summarize the important properties of graphene materials required for their application in neuroscience, the interaction between graphene-based materials and various cells in the central and peripheral nervous systems, and their potential clinical applications in recording electrodes, drug delivery, treatment, and as nerve scaffolds for neurological diseases. Finally, we offer insights into the prospects and limitations to aid graphene development in neuroscience research and nanotherapeutics that can be used clinically.

Abstract Background The major challenge of facing the efficient utilization of biomass is the high cost of cellulolytic enzyme, while the Trichoderma longibrachiatum plays an essential role in the production of industrial enzymes and biomass recycling. Results The cellulase hyper‑producing mutants of LC-M4 and LC-M16 derived from the wild type T. longibrachiatum LC strain through heavy ion mutagenesis exhibited the high-efficiency secretion ability of cellulase and hemicellulose. The FPase activities of LC-M4 (4.51 IU/mL) and LC-M16 (4.16 IU/mL) mutants increased by 46.91% and 35.5% when compared to the LC strain, respectively. Moreover, these two cellulase hyper-producing mutants showed faster growth rate on the cellulosic substrates (Avicel and CMC-Na) plate than that of LC strain. Therefore, an integrative transcriptome and proteome profiling analysis of T. longibrachiatum LC and its cellulase hyper‑producing mutant LC-M4 and LC-M16 were employed to reveal the key genes involved in cellulolytic enzymes regulation. It was showed that the transcriptome and proteome profiles changed dramatically between the wild strain and mutant strains. Notably, the overlapped genes obtained from integrative analysis identified that the protein processing in ER involved in protein secretory pathway, starch and sucrose metabolism pathway and N-glycan biosynthesis pathway were significantly changed both in cellulase hyper-producing mutants and thereby improving the enzyme secretion efficiency, which maybe the main reason of cellulase hyper-production in LC-M4 and LC-M16 mutants. In addition, the three DEGs/DEPs (PDI, Sec61, VIP36) related with protein secretion in ER and two DEGs/DEPs (OST, MOGS) related with N-glycan biosynthesis were identified as key candidate genes participating in enzyme protein biosynthesis and secretion. Conclusions In this study, a hypothetical secretory model of cellulase protein in filamentous fungi was established on the basis of DEGs/DEPs and key genes identified from the omics analysis, which were of great guidance on the rational genetic engineering and/or breeding of filamentous fungi for improving cellulase production.

Abstract UHMK1, a serine/threonine kinase with a U2AF homology motif, is implicated in RNA processing and protein phosphorylation. Increasing evidence has indicated its involvement in tumorigenesis. However, it remains to be elucidated whether UHMK1 plays a role in the development of colorectal cancer (CRC). Here, we demonstrated that UHMK1 was frequently upregulated in CRC samples compared with adjacent normal tissue and high expression of UHMK1 predicted poor outcomes. Knockdown of UHMK1 by siRNAs restrained CRC cell proliferation and increased oxaliplatin sensitivity, whereas overexpression of UHMK1 promoted CRC cell growth and oxaliplatin resistance, suggesting that UHMK1 plays important oncogenic roles in CRC. Mechanistically, we showed that UHMK1 had a significant effect on IL6/STAT3 signaling by interacting with STAT3. The interaction of UHMK1 with STAT3 enhanced STAT3 activity in regulating gene transcription. Furthermore, we found that STAT3 could in turn transcriptionally activate UHMK1 expression in CRC cells. The complementary experiments for cell growth and oxaliplatin resistance indicated the interdependent relationship between UHMK1 and STAT3. Thus, these collective findings uncovered a new UHMK1/STAT3 positive feedback regulatory loop contributing to CRC development and chemoresistance.

Sodium-ion batteries (SIBs) are highly desirable energy storage devices because of their low cost, high safety, and environmental compatibility. Therefore, SIBs have wide application prospects in the fields of large-scale energy storage and electric vehicles. SIBs have a similar energy storage mechanism as that of lithium-ion batteries (LIBs) and can be fabricated using existing LIB production equipment. Thus, SIBs are the most promising alternative to LIBs. However, the radius of Na+ is ~34% larger than that of Li+; therefore, many electrode materials developed for LIBs are unsuitable for SIBs. The exploration of novel electrode materials for SIBs has garnered significant interest in recent years. Among various candidate anode materials for SIBs, red phosphorus is a promising material owing to its ultrahigh theoretical specific capacity (2596 mA·h·g–1), suitable oxidation–reduction potential (0.4 V vs Na/Na+), and abundance. However, the capacity utilization, long-term cycle stability, and rate performance of red phosphorous are limited due to its low intrinsic conductivity and a large volume effect upon sodium storage. At present, an effective approach for the modification of red phosphorus anodes is to prepare nanosized red phosphorus (NRP). Miniaturizing red phosphorus prevents structural damage via large volume changes during charge/discharge processes and also shortens Na+ transmission distances, which enables high electrochemical activity and long-term cycling stability. Herein, recent studies on NRP preparation for advanced SIBs are extensively reviewed. NRP preparation methods typically include ball milling, vaporization condensation, and chemical deposition. Other novel approaches such as thermal reduction, vapor growth, and solvothermal synthesis have also been reported. Ball milling is straightforward and scalable; however, strict guidelines are required to prevent the red phosphorus from burning and exploding, and slight oxidation and particle aggregation are unavoidable. Vaporization-condensation strategies are suitable for the uniform deposition of NRP onto a matrix but are limited by low phosphorus loading and residual white phosphorus. Chemical deposition methods are promising due to their simplicity, control over particle size, and scalability. There are two main chemical deposition strategies, i.e., the reduction of phosphorus-containing compounds and the dissolution and deposition of phosphorus amines. The former method is facile and compatible with ambient temperatures, while the latter method is safe, cost effective, and has high yields. Further studies should focus on morphology design, increasing phosphorus loading, and developing novel chemical reduction methods. We hope that this review promotes the development of red phosphorous anodes for application in SIBs.

Abstract As the most commonly diagnosed lung cancer, non–small cell lung carcinoma (NSCLC) is regulated by many long noncoding RNAs (lncRNAs). In the present study, we found that SH3PXD2A-AS1 expression in NSCLC tissues was upregulated compared with that in normal lung tissues in The Cancer Genome Atlas (TCGA) database by using the GEPIA website. K-M analysis was performed to explore the effects of this molecule on the survival rate in NSCLC. The results demonstrated that SH3PXD2A-AS1 expression was increased in human NSCLC, and high SH3PXD2A-AS1 expression was correlated with poor overall survival. SH3PXD2A-AS1 promotes lung cancer cell proliferation and accelerates cell cycle progression in vitro. Animal studies validated that knockdown of SH3PXD2A-AS1 inhibits NSCLC cell proliferation in vivo. Mechanically, SH3PXD2A-AS1 interacted with DHX9 to enhance FOXM1 expression, promote tumour cell proliferation and accelerate cell cycle progression. Altogether, SH3PXD2A-AS1 promoted NSCLC growth by interacting with DHX9 to enhance FOXM1 expression. SH3PXD2A-AS1 may serve as a promising predictive biomarker for the diagnosis and prognosis of patients with NSCLC.

Abstract Transketolase (TKT) which is an important metabolic enzyme in the pentose phosphate pathway (PPP) participates in maintaining ribose 5-phosphate levels. TKT is necessary for maintaining cell growth. However, we found that in addition to this, TKT can also affect tumor progression through other ways. Our previous study indicate that TKT could promote the development of liver cancer by affecting bile acid metabolism. And in this study, we discovered that TKT expression was remarkably upregulated in colorectal cancer, abnormal high expression of TKT is associated with poor prognosis of colorectal cancer. Additionally, TKT promoted colorectal cancer cell growth and metastasis. Further study demonstrated that TKT interacted with GRP78 and promoted colorectal cancer cell glycolysis through increasing AKT phosphorylation, thereby enhancing colorectal cancer cell metastasis. Thus, TKT is expected to become an indicator for judging the prognosis of colorectal cancer, and provide a theoretical basis for drug development of new treatment targets for colorectal cancer.

Abstract As a promising cathode material of sodium‐ion batteries, Na3V2(PO4)3 (NVP) has attracted extensive attention in recent years due to its high stability and fast Na+ ion diffusion. However, the reversible capacity based on the two‐electron reaction mechanism is not satisfactory limited by the inactive M1 lattice sites during the insertion/extraction process. Herein, self‐supporting 3D porous NVP materials with different crystallinity are fabricated on carbon foam substrates by a facile electrostatic spray deposition method. The V5+/V4+ redox couple is effectively activated and the three‐electron reactions are realized in NVP for sodium storage by a proper crystallinity tuning. In a disordered NVP sample, an ultra‐high specific capacity of 179.6 mAh g−1 at 0.2 C is achieved due to the coexistence of redox reactions of the V4+/V3+ and V5+/V4+ couples. Moreover, a pseudocapacitive charge storage mechanism induced by the disordered structure is first observed in the NVP electrode. An innovative model is given to understand the disorder‐induced‐pseudocapacitance phenomenon in this polyanion cathode material.

Abstract Circular RNAs (circRNAs) are classified as noncoding RNAs because they are devoid of a 5’ end cap and a 3’ end poly (A) tail necessary for cap-dependent translation. However, increasing numbers of translated circRNAs identified through high-throughput RNA sequencing overlapping with polysome profiling indicate that this rule is being broken. CircRNAs can be translated in cap-independent mechanism, including IRES (internal ribosome entry site)-initiated pattern, MIRES (m6A internal ribosome entry site) -initiated patterns, and rolling translation mechanism (RCA). CircRNA-encoded proteins harbour diverse functions similar to or different from host proteins. In addition, they are linked to the modulation of human disease including carcinomas and noncarcinomas. CircRNA-related translatomics and proteomics have attracted increasing attention. This review discusses the progress and exclusive characteristics of circRNA translation and highlights the latest mechanisms and regulation of circRNA translatomics. Furthermore, we summarize the extensive functions and mechanisms of circRNA-derived proteins in human diseases, which contribute to a better understanding of intricate noncanonical circRNA translatomics and proteomics and their therapeutic potential in human diseases.

Abstract. Normal pregnancy is associated with dramatically increased estrogen biosynthesis whose role is believed to raise uterine blood flow to facilitate the bi-directional maternal-fetal exchanges of gases (O2 and CO2), to deliver nutrients, and exhaust wastes to support fetal development and survival. Constrained uterine blood flow in pregnancy is a leading cause of preeclampsia with fetal growth restriction, rendering investigations of uterine hemodynamics to hold a high promise to inform pathways as targets for therapeutic interventions for preeclampsia. The mechanisms of estrogen-induced uterine vasodilation in pregnancy have long been attributed to enhanced endothelium production of nitric oxide, but clinical trials targeting this pathway that dominates uterine hemodynamics have achieved no to little success. Emerging evidence has recently shown a novel proangiogenic vasodilatory role of hydrogen sulfide in regulating uterine hemodynamics in pregnancy and preeclampsia, provoking a new field of perinatal research in searching for alternative pathways for pregnancy disorders especially preeclampsia and intrauterine growth restriction. This minireview is intended to summarize the nitric oxide pathway and to discuss the emerging hydrogen sulfide pathway in modulating estrogen-induced uterine vasodilation in pregnancy and preeclampsia.

Abstract Protein arginine methyltransferase 1 (PRMT1) is able to promote breast cancer cell proliferation. However, the detailed mechanisms of PRMT1-mediated breast cancer cell proliferation are largely unknown. In this study, we reveal that PRMT1-mediated methylation of EZH2 at the R342 site (meR342-EZH2) has a great effect on PRMT1-induced cell proliferation. We also demonstrate that meR342-EZH2 can accelerate breast cancer cell proliferation in vitro and in vivo. Further, we show that meR342-EZH2 promotes cell cycle progression by repressing P16 and P21 transcription expression. In terms of mechanism, we illustrate that meR342-EZH2 facilitates EZH2 binding with SUZ12 and PRC2 assembly by preventing AMPKα1-mediated phosphorylation of pT311-EZH2, which results in suppression of P16 and P21 transcription by enhancing EZH2 expression and H3K27me3 enrichment at P16 and P21 promoters. Finally, we validate that the expression of PRMT1 and meR342-EZH2 is negatively correlated with pT311-EZH2 expression. Our findings suggest that meR342-EZH2 may become a novel therapeutic target for the treatment of breast cancer.

Dissolved gas analysis (DGA) is a common technology used in the on-site maintenance of oil-immersed power transformers in the power industry at present. However, when the content of dissolved gas in the oil reaches the attention value DGA method can effectively diagnose the operating state of the transformer. Due to the lack of gas production data of free gas which was detected when the faults occur, DGA method cannot timely diagnose the transformer status. To solve the above problem, an experimental platform is built for studying the free gas generation law in oil-immersed transformers under discharge faults, and the characteristic free gas information under discharge fault of transformer is obtained through the experiment. It is found that the existing DGA method cannot accurately analyze the types and severity of sudden serious insulation faults. When high-energy partial discharge fault occurred in the equipment, CO, CO2, CH4, and H2 will be collected in large quantities on the oil surface. These four gases can be used as the basis for characterizing high-energy partial discharge faults. When spark discharge occurred in the equipment, C2H6, C2H4, and C2H2 also be collected on the oil surface which can be used as a diagnostic basis for spark discharge. Moreover, it is found that the existing three-ratio method cannot be used for accurate analysis of oil free characteristic gas, so it is necessary to explore new diagnostic methods. The aim of this study is to explore the pattern of free gas production law by experiments when discharge faults occur and to provide data for a new diagnostic method.

In recent years, the calculation of the core grounding current of the converter transformer is difficult, low precision, and time-consuming, especially when the core is grounded by multiple points. This makes it difficult to analyze the core grounding current. To improve the accuracy of the calculation and reduce the complexity of the calculation, this paper carries out analytical calculation, simulation analysis, and experimental research on the grounding current of the converter transformer core. Firstly, a calculation method of core grounding current considering the winding connection of the converter transformer is proposed. In the implementation process, the converter transformer circuit model is established and the influence of saturation characteristics is considered, and the core grounding current is calculated and analyzed. Secondly, the grounding current of the converter transformer core is calculated by the finite element method (FEM). Finally, the proposed scheme is verified by experiments. The results show that the analytical method is close to the FEM and the experimental method, which indicates that the analytical method proposed can meet the accuracy requirements of engineering in this paper, and provides a new scheme for fast and accurate calculation of the grounding current of the converter transformer core.