Actively Tunable "Single Peak/Broadband" Absorbent, Highly Sensitive Terahertz Smart Device Based on VO2.

In recent years, the development of terahertz (THz) technology has attracted significant attention. Various tunable devices for THz waves (0.1 THz-10 THz) have been proposed, including devices that modulate the amplitude, polarization, phase, and absorption. Traditional metal materials are often faced with the problem of non-adjustment, so the designed terahertz devices play a single role and do not have multiple uses, which greatly limits their development. As an excellent phase change material, VO2's properties can be transformed by external temperature stimulation, which provides new inspiration for the development of terahertz devices. To address these issues, this study innovatively combines metamaterials with phase change materials, leveraging their design flexibility and temperature-induced phase transition characteristics. We have designed a THz intelligent absorber that not only enables flexible switching between multiple functionalities but also achieves precise performance tuning through temperature stimulation. Furthermore, we have taken into consideration factors such as the polarization mode, environmental temperature, structural parameters, and incident angle, ensuring the device's process tolerance and environmental adaptability. Additionally, by exploiting the principle of localized surface plasmon resonance (LSPR) accompanied by local field enhancement, we have monitored and analyzed the resonant process through electric field characterization. In summary, the innovative approach and superior performance of this structure provide broader insights and methods for THz device design, contributing to its theoretical research value. Moreover, the proposed absorber holds potential for practical applications in electromagnetic invisibility, shielding, modulation, and detection scenarios.

Hub biomarkers in ultrasound-guided bladder cancer and osteosarcoma: Myosin light chain kinase and caldesmon.

Bladder cancer and osteosarcoma are 2 types of cancers that originate from epithelial tissues inside the bladder and bone or muscle tissues. Ultrasound-guided biopsies provide crucial support for the diagnosis and treatment of bladder cancer and osteosarcoma. However, the relationship between myosin light chain kinase (MYLK) and caldesmon (CALD1) and bladder cancer and osteosarcoma remains unclear. The bladder cancer datasets GSE65635 and GSE100926, the osteosarcoma dataset GSE39058, were obtained from gene expression omnibus. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. The construction and analysis of protein-protein interaction network, functional enrichment analysis, gene set enrichment analysis. Gene expression heat map was drawn and immune infiltration analysis was performed. The comparative toxicogenomics database analysis were performed to find disease most related to core gene. Western blotting experiments were performed. TargetScan screened miRNAs that regulated central DEGs. We obtained 54 DEGs. Functional enrichment analysis revealed significant enrichment in terms of cellular differentiation, cartilage development, skeletal development, muscle actin cytoskeleton, actin filament, Rho GTPase binding, DNA binding, fibroblast binding, MAPK signaling pathway, apoptosis, and cancer pathways. Gene set enrichment analysis indicated that DEGs were primarily enriched in terms of skeletal development, cartilage development, muscle actin cytoskeleton, MAPK signaling pathway, and apoptosis. The immune infiltration analysis showed that when T cells regulatory were highly expressed, Eosinophils exhibited a similar high expression, suggesting a strong positive correlation between T cells regulatory and Eosinophils, which might influence the disease progression in osteosarcoma. We identified 6 core genes (SRF, CTSK, MYLK, VCAN, MEF2C, CALD1). MYLK and CALD1 were significantly correlated with survival rate and exhibited lower expression in bladder cancer and osteosarcoma samples compared to normal samples. Comparative toxicogenomics database analysis results indicated associations of core genes with osteosarcoma, bladder tumors, bladder diseases, tumors, inflammation, and necrosis. The results of Western blotting showed that the expression levels of MYLK and CALD1 in bladder cancer and osteosarcoma were lower than those in normal tissues. MYLK and CALD1 likely play a role in regulating muscle contraction and smooth muscle function in bladder cancer and osteosarcoma. The lower expression of MYLK and CALD1 is associated with poorer prognosis.

KIF20A as a potential biomarker of renal and bladder cancers based on bioinformatics and experimental verification.

BACKGROUND: Bladder cancer (BC) is a malignant tumor that occurs in the bladder wall and often appears in elderly individuals. Renal cancer (RC) arises from the renal tubular epithelium, but its molecular mechanism remains unclear. METHODS: We downloaded RC datasets (GSE14762 and GSE53757) and a BC dataset (GSE121711) to screen differentially expressed genes (DEGs). We also performed weighted gene coexpression network analysis (WGCNA). We created a protein-protein interaction (PPI) network and performed functional enrichment analysis, such as gene set enrichment analysis (GSEA). Heatmaps were made for gene expression. Survival analysis and immunoinfiltration analysis were performed. Comparative toxicogenomics database (CTD) analysis was performed to find the relationship between disease and hub genes. Western blotting was performed to verify the role of KIF20A in apoptosis. RESULTS: A total of 764 DEGs were identified. The GSEA showed that the DEGs were mainly enriched in organic acid metabolism, drug metabolism, mitochondria, and metabolism of cysteine and methionine. The PPI network in GSE121711 showed that KIF20A was a hub gene of renal clear cell carcinoma. Where the expression level of KIF20A was higher, the prognosis of patients was worse. CTD analysis showed that KIF20A was associated with inflammation, proliferation, and apoptosis. KIF20A expression in the RC group was upregulated, as shown by western blotting. The core proteins (including pRB Ser 780, CyclinA, E2F1, CCNE1, and CCNE2) in the pRB Ser 780/CyclinA signaling pathway were also upregulated in the RC group. CONCLUSIONS: KIF20A might be a novel biomarker for researching renal and bladder cancers.

Role of CCT4/ErbB signaling in nephroblastoma: Implications for a biomarker of Wilms tumor.

Wilms tumor is a common abdominal malignant tumor in children. However, the molecular mechanism of Wilms tumor is unclear. GSE66405 and GSE197047 were obtained from the Gene Expression Omnibus database. To identify differentially expressed genes (DEGs) in Wilms tumor, the R package "limma" was used. Weighted gene co-expression network analysis was performed to identify the significant module. The list of DEGs was input into the Search Tool for the Retrieval of Interacting Genes database to construct a protein-protein interaction network for predicting core genes. Gene Ontology analysis and the Kyoto Encyclopedia of Genes and Genomes analysis are computational methods for assessing gene function and biological pathways. The genome was analyzed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes and developed by gene set enrichment analysis. Comparative Toxicogenomics Database analysis was performed to find the diseases most related to the core genes. TargetScan was used to screen for miRNAs that regulate hub genes. A total of 925 DEGs were identified. The differently expressed genes were mainly enriched in the metabolic pathway, AMPK signaling pathway, ErbB signaling pathway, mRNA detection pathway, and folded protein binding. A total of 16 core genes (HNRNPK, PABPC1, HNRNPD, NCL, YBX1, EIF4G1, KHDRBS1, HNRNPAB, HSPA4, EEF2, HSP90AA1, EEF1A1, A TP5A1, SDHA, CCT4, CCT5) were obtained. chaperonin containing TCP-1 subunit 4 (CCT4) was downregulated in tumor tissue samples, which may have reverse regulatory significance for Wilms tumor. CCT4, HSP90AA1, NCL, PABPC1, and YBX1 were found to be associated with kidney disease, acute kidney injury, edema, tumor metastasis, transitional cell carcinoma, necrosis, and inflammation. The research found that the related miRNA of the CCT4 gene was hsamiR-7-5p. CCT4 might play an essential role in the occurrence and development of Wilms tumor, and they may participate in the occurrence and development of Wilms tumor through the ERBB signal pathway. CCT4 may be a promising biomarker of Wilms tumor.

CCNB2 as a potential biomarker of bladder cancer via the high throughput technology.

Bladder cancer and oral squamous cell carcinoma (OSCC) seriously affect people's health. However, the relationship between bladder cancer and OSCC remains unclear. Got GSE138206, GSE146483, GSE184616, and bladder cancer datasets GSE65635, GSE100926 from Gene Expression Omnibus database. Weighted gene co-expression network analysis was used to identify the significant module. Functional enrichment analysis was performed via the Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes. Furthermore, the Gene Set Enrichment Analysis was also used to complete the enrichment analysis. Comparative Toxicogenomics Database found most relevant diseases to core genes. TargetScan is used to forecast analysis of microRNA and target genes. In Gene Ontology analysis, differentially expressed genes were mostly concentrated in cell differentiation, extrallular region, structural molecule activity, and actin binding. In Kyoto Encyclopedia of Genes and Genomes analysis, the differentially expressed genes were mainly enriched in PI3K-Akt signaling pathway, pathway in cancer, and extracellular matrix-receptor interaction. Seven hub genes (cyclin B2 [CCNB2], TK1, CDC20, PCNA, CKS1B, CDCA5, MCM4) were obtained. Hub genes (CCNB2, CDC20) are highly expressed in OSCC and bladder cancer samples. CCNB2 was one common oncogene of bladder cancer and OSCC.

High expression of KIF20A in bladder cancer as a potential prognostic target for poor survival of renal cell carcinoma.

Urinary system tumors are malignant tumors, including renal cancer and bladder cancer. however, molecular target of them remains unclear. GSE14762 and GSE53757 were downloaded from GEO database to screen differentially expressed genes (DEGs). Weighted gene co-expression network analysis was performed. Gene Ontology (GO) and Kyoto encyclopedia of genes and genomes were used for enrichment analysis. Gene ontology and Kyoto encyclopedia of genes and genomes analyses were performed on whole genome, as formulated by gene set enrichment analysis. Survival analysis was also performed. Comparative toxicogenomics database was used to identify diseases most associated with hub genes. A total of 1517 DEGs were identified. DEGs were mainly enriched in cancer pathway, HIF-1 signaling pathway, organic acid metabolism, glyoxylate and dicarboxylate metabolism, and protein homodimerization activity. Ten hub genes (TPX2, ASPM, NUSAP1, RAD51AP1, CCNA2, TTK, PBK, MELK, DTL, kinesin family member 20A [KIF20A]) were obtained, which were up-regulated in tumor tissue. The expression of KIF20A was related with the overall survival of renal and bladder cancer. KIF20A was up-regulated in the tumor tissue, and might worsen the overall survival of bladder and kidney cancer. KIF20A could be a novel biomarker of bladder and kidney cancer.

KLK4 Silencing Inhibits the Growth of Chromophobe Renal Cell Carcinoma through ERK/AKT Signaling Pathway.

INTRODUCTION: Renal cell carcinoma (RCC) generally has a poor prognosis because of late diagnosis and metastasis. Despite its abundance in RCC cells, the functions of kallikrein-related peptidase 4 (KLK4) in RCC cells remain unknown. The results of this investigation were examined to discover if KLK4 gene silencing influences the development of RCC cells. METHODS: The mRNA levels of KLK4 and the relationship between KLK4 and tumor stage in patients with RCC were analyzed from the GEPIA database. Real-time PCR and Western blotting were used to measure the mRNA and protein levels of KLK4. Cell Counting Kit 8 (CCK-8), colony formation, wound healing, and Transwell assays were used to examine the proliferation, invasion, and migration of RCC cells after KLK4 suppression. Finally, xenograft experiments in a mouse model helped understand the in vivo effects of KLK4 knockdown. RESULTS: Our research found that KLK4 expression was upregulated in the kidney chromophobe (KICH) specimens and cell lines. Moreover, inhibiting KLK4 growth led to a slowdown in RCC cell proliferation and colony formation. Additionally, KLK4 knockdown inhibited migration, invasion, and epithelial-mesenchymal transition (EMT) of RCC cells. AKT and ERK phosphorylation were enhanced with KLK4 silencing. In the nude mouse xenograft cancer model, KLK4 silencing also prevented the expression of Ki-67, CD105, and the growth of tumors. CONCLUSION: KLK4 accelerated KICH progression via the ERK/AKT signaling pathway, providing a novel regulatory mechanism for KICH pathogenesis.

PLK1 as one novel target for the poor prognosis of bladder cancer: An observational study.

Bladder cancer (BC) is one of the most common male malignant tumors and the most common urological tumor. However, the molecular mechanism and role of PLK1 on bladder cancer were unclear. Therefore, the study aims to explore the potential part of the overall survival of bladder cancer through bioinformatics analysis. GSE121711 and GSE130598, from the Gene Expression Omnibus database. The GEO2R screened differently expressed genes, and DAVID and Metascape were used for functional annotation. The cytoHubba made hub genes identification and expression. A total of 50 BC participants were recruited. After surgery, 50 BC tumor samples from BC patients and 50 adjacent standard bladder tissue samples were obtained. The RT-qPCR assay was performed to verify the expression of hub genes. The Kaplan-Meier Plotter analyzed the effect of hub gene expression for overall survival of BC. The compulsory module of Molecular Complex Detection tool analysis was shown, which included CDK1, TTK, AURKB, MELK, PLK1, and BUB1. And the six hub genes were up-regulated in the BC compared with the normal tissues. The relative expression levels of CDK1, TTK, AURKB, MELK, PLK1, and BUB1 were significantly higher in BC samples compared with the regular kidney tissue groups. The result demonstrated that CDK1, TTK, AURKB, MELK, PLK1, and BUB1 might be considered biomarkers for BC. Overall survival analysis showed that BC patients with high expression level of PLK1 had poorer overall survival times than those with low expression level (P < .05). The expression levels of CDK1, TTK, AURKB, MELK, and BUB1 was not related to the overall survival of BC patients (P > .05). The PLK1 gene might provide new ideas and evidence for bladder cancer research.

Long Noncoding RNA MMP2-AS1 Contributes to Progression of Renal Cell Carcinoma by Modulating miR-34c-5p/MMP2 Axis.

Renal cell carcinoma (RCC) serves as a prevalent malignancy of urinary system and presents severe mortality and increasing incidence. Long noncoding RNAs (lncRNAs) have demonstrated critical roles in RCC development. Here, we were interested in the function of MMP2-AS1 during RCC progression. We observed that MP2-AS1 localized in both nucleus and cytoplasm of RCC cells using fluorescent in situ hybridization (FISH). The cell viability, proliferation, invasion, and migration of RCC cells were reduced by the depletion of MMP2-AS1. The MMP2-AS1 depletion-inhibited viability, proliferation, migration, and invasion of RCC cells were rescued by the overexpression of MMP2 in vitro. Consistently, the tumor growth of RCC cells was repressed by the depletion of MMP2-AS1 in the nude mice, while the overexpression of MMP2 could reverse this effect in vivo. Mechanically, we predicted the potential interaction of miR-34c-5p with both MMP2-AS1 and MMP2. The treatment of miR-34c-5p mimic reduced the luciferase activity of MMP2-AS1 and MMP2 3'UTR. The depletion of MMP2-AS1 enhanced miR-34c-5p expression and the expression of MMP2 was inhibited by miR-34c-5p in RCC cells. The protein levels of MMP2 were downregulated by MMP2-AS1 knockdown, while the inhibitor of miR-34c-5p rescued the expression of MMP2 in the cells. The treatment of miR-34c-5p mimic attenuated the cell viability, proliferation, invasion, and migration of RCC cells, in which MMP2 overexpression restored the phenotypes. MMP2-AS1 depletion-attenuated viability, proliferation, migration, and invasion of RCC cells were reversed by miR-34c-5p inhibitor. We concluded that MMP2-AS1 contributed to progression of renal cell carcinoma by modulating miR-34c-5p/MMP2 axis.

Broadband Solar Absorber Based on Square Ring cross Arrays of ZnS.

Solar energy is an inexhaustible clean energy. However, how to improve the absorption efficiency in the visible band is a long-term problem for researchers. Therefore, an electromagnetic wave absorber with an ultra-long absorption spectrum has been widely considered by researchers of optoelectronic materials. A kind of absorbing material based on ZnS material is presented in this paper. Our purpose is for the absorber to achieve a good and wide spectrum of visible light absorption performance. In the wide spectrum band (553.0 THz-793.0 THz) of the absorption spectrum, the average absorption rate of the absorber is above 94%. Using surface plasmon resonance (SPR) and gap surface plasmon mode, the metamaterial absorber was studied in visible light. In particular, the absorber is insensitive to both electric and magnetic absorption. The absorber can operate in complex electromagnetic environments and at high temperatures. This is because the absorber is made of refractory metals. Finally, we discuss and analyze the influence of the parameters regulating the absorber on the absorber absorption efficiency. We have tried to explain why the absorber can produce wideband absorption.

Knockdown of PLOD3 suppresses the malignant progression of renal cell carcinoma via reducing TWIST1 expression.

Procollagen-lysine, 2-oxoglutarate 5-dioxygenase (PLOD3), also known as lysyl hydroxylase 3 (LH3) has been demonstrated to be overexpressed in several kinds of cancers and facilitate cell migration. Currently, we aimed to reveal the role of PLOD3 in renal cell carcinoma (RCC) progression, and explore whether TWIST1 (Twist family bHLH transcription factor 1) is involved in this process. Fifty-eight paired RCC tissues and normal tissues were collected and subjected to qPCR and immunohistochemistry (IHC) technology to detect the expression levels of PLOD3. The clinical value of PLOD3 in predicting RCC progression was then explored. Cell-Counting Kit-8 (CCK-8), wound healing, transwell chambers and tumor-bearing experiments were applied to monitor cell proliferation, migration, invasion and tumorigenesis. Protein levels were determined by using western blotting technology to assess cell apoptosis and epithelial to mesenchymal transition (EMT). PLOD3 expression was enhanced in RCC tissues and cells, which predicted higher T (tumor), N (lymph node) and M (metastasis) stages, histological grade and TNM (tumor, lymph node, metastasis) stage. PLOD3 downregulation in RCC A498 cells obviously inhibited cell proliferation, migration, invasion, EMT and tumorigenesis and increased cell apoptosis. PLOD3 overexpression led to opposite results in RCC A704 cells. PLOD3 downregulation reduced the expression levels of TWIST1, ß-catenin and p-AKT. In addition, TWIST1 overexpression rescued the repressions of cell proliferation, migration, invasion, EMT and the activation of ß-catenin and AKT signaling in addition to apoptosis promotion induced by PLOD3 downregulation. Collectively, this study illustrated that PLOD3 knockdown suppressed RCC malignance via inhibiting TWIST1-mediated activation of ß-catenin and AKT signaling.

Radioimmunoimaging of colorectal cancer using (99m)Tc labeled monoclonal antibody.

AIM:To determine whether Hb3 and its fragment F(ab')(2) have practical value in radioimmunoimaging of colorectal cancer.METHODS:Intact Hb3 was purified by hydroxylapatite chromatography.The fragment F(ab') (2) was prepared by cold digestion and purified as intact Hb3.Hb3 and its fragment F(ab') (2) were labeled with 99mTc by direct labeling method using SnCl(2) as reducing agent. The radioactive doses ranged from 15 to 40 mCi.The imaging was accomplished by single photon emission computered tomograph (SPECT) with imaging time ranging from 2.5 to 48 hours. In this study, 10 patients were selected. Among them, 7 were administered with intact Hb3, and 3 with F(ab') (2) fragment. All the patients were diagnosed as having colorectal adenocarcinoma.RESULTS:After purification, intact Hb3 and its fragment F(ab') (2) were fit for radioimmunoimaging. The percentage of labeling of (99m)Tc to Hb3 or F(ab') (2) was 80.6%-91.5%. Among the 10 patients, 3 of 7 patients administered with intact Hb3 had positive scans, the other 4 had negative scans, and 2 of 3 patients administered with F(ab') (2)had positive scans, the other 1 had negative scans.CONCLUSION:The results showed that both intact Hb3 and its F(ab') (2) have some practical value in radioimmunoimaging of colorectal cancer, and the effects of imaging with F(ab') (2) was better than that with intact Hb3.