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Hybrid quantum systems based on magnons in magnetic materials have made significant progress in the past decade. They are built based on the couplings of magnons with microwave photons, optical photons, vibration phonons, and superconducting qubits. In particular, the interactions among magnons, microwave cavity photons, and vibration phonons form the system of cavity magnomechanics (CMM), which lies in the interdisciplinary field of cavity QED, magnonics, quantum optics, and quantum information. Here, we review the experimental and theoretical progress of this emerging field. We first introduce the underlying theories of the magnomechanical coupling, and then some representative classical phenomena that have been experimentally observed, including magnomechanically induced transparency, magnomechanical dynamical backaction, magnon-phonon cross-Kerr nonlinearity, etc. We also discuss a number of theoretical proposals, which show the potential of the CMM system for preparing different kinds of quantum states of magnons, phonons, and photons, and hybrid systems combining magnomechanics and optomechanics and relevant quantum protocols based on them. Finally, we summarize this review and provide an outlook for the future research directions in this field.

Using phonons to simulate an optical two-level laser action has been the focus of research. We theoretically study phonon laser in a cavity magnomechanical system, which consist of a microwave cavity, a sphere of magnetic material and a uniform external bias magnetic field. This system can realize the phonon-magnon coupling and the cavity photon-magnon coupling via magnetostrictive interaction and magnetic dipole interaction respectively, the magnons are driven directly by a strong microwave field simultaneously. Frist, the intensity of driving magnetic field which can reach the threshold condition of phonon laser is given. Then, we demonstrate that the adjustable external magnetic field can be used as a good control method to the phonon laser. Compared with phonon laser in optomechanical systems, our scheme brings a new degree of freedom of manipulation. Finally, with the experimentally feasible parameters, threshold power in our scheme is close to the case of optomechanical systems. Our study may inspire the field of magnetically controlled phonon lasers.

Tripartite motif-containing 3 (TRIM 3), as a vital member of TRIM family, has been receiving significant attention in cancer research. This research aims to detect the effect and relevant molecular functions of TRIM3 in melanoma cells.GEPIA website and immunohistochemical analysis were performed to investigate TRIM3 level in melanoma samples. The growth ability, the mobility, and the apoptosis of M14 and A375 cells were determined by biological experiments. qPCR and western blot assays were performed to evaluate the expression of key genes. The interaction between TRIM3 and YAP1 was verified by immunoprecipitation and ubiquitination assays.A reduction of TRIM3 was observed in melanoma samples, and the loss of TRIM3 strengthened the proliferation and mobility of M14 and A375 cells and diminished apoptosis, and vice versa. TRIM3 expression only affected the protein level of YAP1, while YAP1 mRNA was not changed. Then, we demonstrated that TRIM3 directly interacted with YAP1, and TRIM3 reduced YAP1 stability by inducing ubiquitination modification. Finally, rescue assays showed that si-YAP1 treatment alleviated the effects of si-TRIM3 on melanoma cells.This study indicated that depletion of TRIM3 strengthened the proliferation and mobility of M14 and A375 cells, suppressed cell apoptosis, but these phenomena were counteracted by YAP1 down-regulation.

Bladder cancer, a highly fatal disease, poses a significant threat to patients. Positioned at 19q13.2-13.3, LIG1, one of the four DNA ligases in mammalian cells, is frequently deleted in tumour cells of diverse origins. Despite this, the precise involvement of LIG1 in BLCA remains elusive. This pioneering investigation delves into the uncharted territory of LIG1's impact on BLCA. Our primary objective is to elucidate the intricate interplay between LIG1 and BLCA, alongside exploring its correlation with various clinicopathological factors. We retrieved gene expression data of para-carcinoma tissues and bladder cancer (BLCA) from the GEO repository. Single-cell sequencing data were processed using the \"Seurat\" package. Differential expression analysis was then performed with the \"Limma\" package. The construction of scale-free gene co-expression networks was achieved using the \"WGCNA\" package. Subsequently, a Venn diagram was utilized to extract genes from the positively correlated modules identified by WGCNA and intersect them with differentially expressed genes (DEGs), isolating the overlapping genes. The \"STRINGdb\" package was employed to establish the protein-protein interaction (PPI) network.Hub genes were identified through the PPI network using the Betweenness Centrality (BC) algorithm. We conducted KEGG and GO enrichment analyses to uncover the regulatory mechanisms and biological functions associated with the hub genes. A machine-learning diagnostic model was established using the R package \"mlr3verse.\" Mutation profiles between the LIG1^high and LIG1^low groups were visualized using the BEST website. Survival analyses within the LIG1^high and LIG1^low groups were performed using the BEST website and the GENT2 website. Finally, a series of functional experiments were executed to validate the functional role of LIG1 in BLCA. Our investigation revealed an upregulation of LIG1 in BLCA specimens, with heightened LIG1 levels correlating with unfavorable overall survival outcomes. Functional enrichment analysis of hub genes, as evidenced by GO and KEGG enrichment analyses, highlighted LIG1's involvement in critical function such as the DNA replication, cellular senescence, cell cycle and the p53 signalling pathway. Notably, the mutational landscape of BLCA varied significantly between LIG1 and LIG1 groups.Immune infiltrating analyses suggested a pivotal role for LIG1 in immune cell recruitment and immune regulation within the BLCA microenvironment, thereby impacting prognosis. Subsequent experimental validations further underscored the significance of LIG1 in BLCA pathogenesis, consolidating its functional relevance in BLCA samples. Our research demonstrates that LIG1 plays a crucial role in promoting bladder cancer malignant progression by heightening proliferation, invasion, EMT, and other key functions, thereby serving as a potential risk biomarker.

Chen's Peiyuan Tang (CSPYT) is a compound herbal formula that has shown the potential to enhance ovarian function and reduce autophagy in ovarian granulosa cells, which plays a crucial role in follicular development and maturation. The application of Chinese herbal medicine offers a promising alternative to traditional hormone replacement therapy (HRT). This study explores CSPYT's therapeutic mechanisms in treating POF, focusing on its modulation of autophagy through network pharmacology and transcriptomics-based analysis, predicting potential interactions and pathways. KGN cell line and rat ovarian granulosa cells were used for experiment. 4-Hydroperoxy cyclophosphamide(4-HC) stimulation was carried out for establishing the POF cell model. Q-PCR, Western Blot, Transmission electron microscopy to detect the results. According to the drug and disease database, the common targets of Chen's Peiyuan Tang and premature ovarian failure were screened, combined with autophagy gene targets and transcriptome analysis, and finally 8 intersection targets were obtained, namely CDKN1B, MAPK3, PRKCD, CDKN1A, MAPK1, RAF1, BIRC5, CTSB. Enrichment analysis of 8 genes found that they were closely related to the animal autophagy pathway. Construct PPI network diagram. CytoScape 3.9.1 builds CSPYT Drug Target-POF Disease Target-Autophagy Gene Network Diagram. Based on the PPI network diagram and CytoScape 3.9.1 analysis results, it is estimated that MAPK1 and MAPK3 are the key targets of CSPYT in the treatment of POF. The eight final intersection targets were docked with the corresponding active pharmaceutical ingredients. The one that docked most closely with the MAPK family was naringenin. In cell experiment verification, it was confirmed that Chen's Peiyuan Tang can inhibit the MAPK signaling pathway, significantly reduce the number of autophagosomes, and reduce autophagy damage in ovarian granulosa cells. CSPYT can inhibit the MAPK signaling pathway, prevent autophagy overexpression and restore ovarian granulosa cell function, effectively alleviating the disease pressure of POF.

Objective False positive and negative results are associated with biliary tract cell brushing cytology during endoscopic retrograde cholangiopancreatography (ERCP). The causes are uncertain. The purpose of this study was to evaluate the accuracy of diagnoses made via cell brushing in our center, and to explore the factors influencing diagnosis. Methods The clinical data of patients who underwent cell brushing at our center from January 2016 to August 2019 were retrospectively analyzed. These included age, gender, stricture location, thickness of the bile duct wall in the narrow segment, maximum diameter of the biliary duct above the stricture, number of cell brush smears, carbohydrate antigen 19-9, and carcinoembryonic antigen. Positive brush cytology results were compared with results of surgical histology or tumor biopsy as well as with the patient’s clinical course. Results Of the 48 patients who underwent cell brushing cytology, 27 (56.3%) had positive results. The sensitivity and specificity of biliary duct cell brushing was 79.4%, and 85.7%, respectively. None of the above-mentioned factors were associated with positive cytology brushing results. Conclusions Cell brushing cytology remains a reliable method for diagnosis of pancreaticobiliary malignancies.

Background Apoptosis and apoptotic genes play a critical role in the carcinogenesis and progression of bladder cancer. However, there is no prognostic model established by apoptotic genes. Methods Messenger RNA (mRNA), Expression data, and related clinical data were obtained from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database. After extracting the apoptosis-related genes, the survival-related apoptosis genes were screened by univariate Cox regression analysis in the TCGA cohort. Following the Least Absolute Shrinkage and Selection Operator (LASSO) regression method, these genes were modeled by multivariate Cox analysis. The predictive abilities of the Apoptosis-Related Gene Model (ARGM) for overall survival (OS) rate, disease-specific survival (DSS) measures, and progression-free survival (PFS) were verified by the Kaplan–Meier(K-M)survival analysis and time-dependent Receiver Operating Characteristic (ROC) curve. Functional enrichment analyses were performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG). CIBERSORT and Single-Sample Gene Set Enrichment Analysis (ssGSEA) were used to calculate the type of immune cell infiltration and immune functions. The model’s predictive ability for immunotherapy were evaluated using Tumor Immune Dysfunction and Exclusion (TIDE) and the Imvigor210 study.The single-cell sequencing was used to display the expression level of the ARGM.Finally,qRT-PCR was executed to validate the expression level of ARGM. Results Several apoptosis genes were identified through the model, including ANXA1, CASP6, CD2, F2, PDGFRB, SATB1, and TSPO. The prognostic value of the model for OS, DSS, and PFS were verified using the TCGA and GEO cohort. The model can predict patient response to immunotherapy treatment as established through the model’s score which was linked to different types of immune cell infiltration and identified significant differences in the signal pathways between high-risk and low-risk groups. Nomogram variables, prompted from ARGM and clinical parameters, also generate a high predictive value for patient survival. Conclusion Ourestablished apoptosis-related gene model (ARGM) has a substantial predictive value for prognosis and immunotherapy of bladder cancer. It may help with clinical consultation, clinical stratification, and treatment selection. The immune infiltration status and signal pathway of different risk groups also provide direction for further research.

Background Cutaneous malignant melanoma is a very aggressive and metastatic form of skin cancer, typically linked with poor outcomes. Advances in genomic analysis have underscored the crucial role of T cells in tumor immunity. Immune checkpoint inhibitors have notably transformed melanoma treatment by boosting T cell activity. Studies of gene expression have found that the phosphatidylinositol-4-phosphate kinase 2A (PIP4K2A) gene is abnormally expressed in various tumors, indicating its potential role in tumor progression. Utilizing single-cell sequencing and machine learning, researchers can now explore the complex interactions between T cells and melanoma cells at a genomic level. This study aimed to investigate the role of the PIP4K2A gene in cutaneous malignant melanoma, with a focus on its influence on T cell-mediated immune responses. Methods Samples from cutaneous melanoma patients were analysed by single-cell transcriptome for differentially expressed genes and signalling pathways associated with cutaneous melanoma. Then, genes were identified and predictive models were built based on the transcriptomic data using machine learning models to assess whether the expression level of PIP4K2A could effectively predict the malignancy and prognosis of cutaneous melanoma. In addition, we also performed drug therapy predictive analysis and immunotherapy analysis.Finally, the critical role of PIP4K2A in cutaneous melanoma was further confirmed by immunohistochemistry. Results The PIP4K2A gene exhibited a significantly elevated expression level in cutaneous malignant melanoma, showing a strong correlation with the clinical stage and patient prognosis. At the therapeutic level, high PIP4K2A expression is less responsive to immunotherapy, and this gene is a risk factor for drug therapy in cutaneous malignant melanoma. Additionally, our experimental outcomes validated this observation. Conclusions The PIP4K2A gene could be a crucial prognostic marker for cutaneous malignant melanoma, as it significantly affects T cell activity within the tumor microenvironment. This study offers essential insights into melanoma pathogenesis and assists in pinpointing new early diagnostic markers and therapeutic targets. Utilizing advanced genomic tools and computational techniques, the research enhances our understanding of T cell dynamics in melanoma, facilitating the development of personalized medicine and more effective immunotherapy strategies.

: Liver cancer with portal vein tumor thrombus (PVTT) indicates a serious prognosis. The molecular mechanism of PVTT formation is not totally clarified, the invasion of blood vessels by liver cancer cells is the key step and portal vein endothelial cells plays critical role. : Conditioned medium (CM) of human umbilical vein endothelial cells (HUVEC) were used to culture liver cancer cells and prostate cancer cells for cell motility and viability analysis for the purpose of simulating the role of macrovascular endothelial cells in the development of liver cancer. : HUVEC-CM caused long spindle-shaped changes in liver cancer cells; the invasion and migration ability of Bel-7402 and MHCC-LM3 (cultured in HUVEC-CM) increased significantly. Integrins/FAK (focal adhesion kinase) signaling pathway was activated and MMP-3 was up-regulated. However, classical epithelial-mesenchymal transition (EMT) did not involve. HUVEC-CM caused a decrease of cell population in G1- and S-phase of Bel-7402, it also caused an accumulation of cell population in G1 phase and a decrease of cell population in S-phase of MHCC-LM3, MHCC-97L and DU-145. HUVEC-CM promotes apoptosis of Bel-7402 and MHCC-97L and the nude mouse tumorigenic experiment did not find that the HUVEC-CM increase the tumorigenic ability of liver cancer cells. : HUVEC may provide an easy-to-adhere roadbed for liver cancer cells invasion of blood vessels by altering extracellular matrix (ECM), activating integrins/FAK pathway and inducing non-classical EMT. The effect of HUVEC-CM on cell viability was cancer cell type dependent. It is a meaningful glance at the mechsanism of PVTT.

Current opinion suggests that expansion of cancer stem cells (CSCs) and activation of pro-tumoral inflammation cascade correlate with cancer progression. We explored the possible contributions of MRC-5 cancer-associated fibroblasts to the expression profiles of CSC markers and inflammation-associated cell surface molecules. The liver cancer cell lines Bel-7402, SMMC-7721, MHCC-LM3, and HepG2 cultured in conditioned medium (CM) from MRC-5 served as test groups, whereas the liver cancer cell lines cultured in normal medium served as control groups. Flow cytometry revealed that the proportions of CD90 cells were significantly higher in MHCC-LM3-(MRC-5)-CM and HepG2-(MRC-5)-CM cells, and moderately higher in Bel-7402-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells, than in controls. The CD90 /CD45 proportions were elevated in Bel-7402-(MRC-5)-CM and MHCC-LM3-(MRC-5)-CM cells, but reduced in HepG2-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells, as compared to controls. Western blotting indicated that Nanog was downregulated in MHCC-LM3-(MRC-5)-CM and HepG2-(MRC-5)-CM cells, compared to controls; that POU5F1 (OCT4/3) was downregulated in MHCC-LM3-(MRC-5)-CM, but upregulated in Bel-7402-(MRC-5)-CM and HepG2-(MRC-5)-CM cells, compared to controls, and that CK19 was upregulated in Bel-7402-(MRC-5)-CM and MHCC-LM3-(MRC-5)-CM cells, compared to controls. Proportions of cells expressing Toll-like receptor-1 (TLR1) and TLR4 were significantly higher in MHCC-LM3-(MRC-5)-CM cells, and moderately higher in HepG2-(MRC-5)-CM cells, than controls. However, the TLR1 and TLR4 proportions were lower in Bel-7402-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells than controls. Proportions of CD25 cells were reduced in HepG2-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells, but elevated in MHCC-LM3-(MRC-5)-CM and Bel-7402-(MRC-5)-CM cells, compared to controls. Proportion of CD61 cells was higher in liver cancer cells cultured in MRC-5-CM than in controls. Proportion of CD14 cells was lower in HCC cells cultured in MRC-5-CM than in controls. MRC-5 extensively affected the production of CSC markers and inflammation-associated cell surface molecules. Tumor-targeting molecular therapies should consider these findings.