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In remote sensing image fusion, the conventional Convolutional Neural Networks (CNNs) extract local features of the image through layered convolution, which is limited by the receptive field and struggles to capture global features. Transformer utilizes self-attention to capture long-distance dependencies in images, which has a global receptive field, but the computational cost for high-resolution images is excessively high. In response to the above issues, this paper draws inspiration from the FusionNet network, harnessing the local detail acquisition capability of CNNs and the global data procuring capacity of Transformer. It presents a novel method for remote sensing image sharpening named Guided Filtering-Cross Stage Partial Network-Transformer, abbreviated as GF-CSTNet. This solution unifies the strengths of Guided Filtering (GF), Cross Stage Partial Network (CSPNet), and Transformer. Firstly, this method utilizes GF to enhance the acquired remote sensing image data. The CSPNet and Transformer structures are then combined to further enhance fusion performance by leveraging their respective advantages. Subsequently, a Rep-Conv2Former method is designed to streamline attention and extract diverse receptive field features through a multi-scale convolution modulator block. Simultaneously, a reparameterization module is constructed to integrate the multiple branches generated during training into a unified branch during inference, thereby optimizing the model's inference speed. Finally, a residual learning module incorporating attention has been devised to augment the modeling and feature extraction capabilities of images. Experimental results obtained from the GaoFen-2 and WorldView-3 datasets demonstrate the effectiveness of the proposed GF-CSTNet approach. It effectively extracts detailed information from images while avoiding the problem of spectral distortion. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effect of doublecortin-like kinase 1 (DCLK1) on the biological properties of gastric cancer stem cells, and to explore its possible mechanism. METHODS: Serum-free suspension culture of gastric cancer stem cells and targeted inhibition of DCLK1 activity in gastric cancer stem cells with DCLK1 inhibitor DCLK1-IN-1 were performed. The expression levels of DCLK1, stemness-related proteins (SOX2 and OCT4), proliferation-related proteins (cyclin D1 and c-MYC), drug resistance-related proteins (ABCG2 and TOP2A), epithelial-mesenchymal transition-related proteins (E-cadherin, vimentin and Snail), and PI3K/AKT/mTOR signaling pathway-related proteins in gastric cancer stem cells were examined by Western blot. The effects of DCLK1 on viability and drug resistance of gastric cancer stem cells were determined by CCK-8 assay, and the effects of DCLK1 on self-renewal of gastric cancer stem cells were determined by methylcellulose spheroid-forming assay. Wound-healing and Transwell assays were performed to assess the effect of DCLK1 on the migration and invasion of gastric cancer stem cells. RESULTS: The expression levels of DCLK1 and stemness-related proteins SOX2 and OCT4 in gastric cancer stem cells were significantly higher than those in parental cells (P<0. 01). The proliferation, drug resistance, migration and invasion of gastric cancer stem cells in DCLK1 inhibition group were significantly lower than those in Sphere cell group (P<0. 01). The expression levels of proliferation-related proteins (c-MYC and cyclin D1) and drug resistance-related proteins (TOP2A and ABCG2) were down-regulated, the expression of epithelial marker E-cadherin was up-regulated, the expression of mesenchymal markers vimentin and Snail was down-regulated, and the expression levels of PI3K/AKT/mTOR signaling pathway-related proteins and their phosphorylation levels were reduced in DCLK1 inhibition group (P<0. 05). CONCLUSION: DCLK1 is highly expressed in gastric cancer stem cells, which may be involved in the proliferation, drug resistance and invasion of gastric cancer stem cells by regulating PI3K/AKT/mTOR signaling pathway. It suggests that DCLK1 can be used as a potential target for gastric cancer stem cells. [ABSTRACT FROM AUTHOR]

AbstractA novel square hierarchical structure axially varying thickness (SHSAVT) structure, drawing inspiration from origami, has been introduced. And a systematic numerical analysis has been conducted to assess the crashworthiness of this innovative structure when subjected to axial impacts. The findings of the crashworthiness analysis demonstrate that SHSAVT structures with k values greater than zero exhibit a remarkable capacity for energy absorption (EA) while maintaining the same mass, and they notably reduce the initial peak crushing force (IPCF). Additionally, it was observed that as the hierarchy level increases, the action force experiences less fluctuation, resulting in increased EA, thus enhancing the overall crashworthiness of the structure while reducing IPCF. Moreover, when compared to structures with the same wall thickness, SHSAVT with k values greater than zero demonstrated a substantial 54.46% decrease in maximum IPCF and a significant 112.27% increase in maximum crushing force efficiency (CFE). Furthermore, higher k values correlated with lower IPCF and higher CFE, SHSAVT with k values greater than zero as superior in terms of IPCF and CFE performance. [ABSTRACT FROM AUTHOR]

Objectives: MicroRNAs possess essential effects on gastric cancer (GC), whereas the underlying mechanisms have not been fully uncovered. The present work focused on investigating the role of miR-381-3p in GC cellular processes and the possible mechanisms. Materials and Methods: miR-381-3p levels within GC tissues and cells were measured through quantitative real-time polymerase chain reaction (qRT-PCR). This study measured cell proliferation, apoptosis, and metastasis through EdU, colony formation, flow cytometry, and Transwell assays separately. TargetScan was adopted to predict the miR-381-3p targets, whereas luciferase reporter assay was adopted for confirmation. Results: miR-381-3p levels were decreased, whereas fibroblast growth factor receptor-2 (FGFR2) expression was increased in GC. miR-381-3p upregulation inhibited proliferation, migration, and invasion and it promoted the apoptosis of GC cells. Further, FGFR2 overexpression partly reversed the miR-381-3p-mediated impacts on GC cellular processes. Conclusions: This study provides an experimental basis, suggesting the potential of using miR-381-3p as the novel marker for GC. Clinical Trial Registration number: 2020-05. [ABSTRACT FROM AUTHOR]

This article presents a four-element phased-array transceiver (TRX) front-end for millimeter-wave (mm-Wave) 5G new radio (NR). The effects of amplitude-to-phase (AM–PM) and amplitude-to-amplitude (AM–AM) distortions on error vector magnitude (EVM) are detailed. A three-stage highly linear wideband class-AB power amplifier (PA) is described, mitigating AM–PM and AM–AM distortions without degrading other performances. A matching network embedded transmitting/receiving (T/R) switch is proposed to support time division duplex (TDD). With the proposed technique, RF switch insertion losses are reduced in both transmitter (TX) and receiving (RX) modes. In each TRX element, phase and gain controls are achieved by a 6-bit vector-modulated phase shifter (VMPS) with a phase tuning range of 360° and a 6-bit attenuator with a gain tuning range of 31.5 dB, respectively. Fabricated in 65-nm bulk CMOS, the proposed packaged TRX demonstrates the measured peak gains of 25.5/14.2 dB with the gain ripples of less than 2.5/1.9 dB across 24–29.5 GHz in the TX/RX mode. The measured peak $P_{\text {1 dB}}$ is 17.6 dBm with a power added efficiency (PAE) of 20.4%. The measured minimum noise figure (NF) is 4.3 dB. The TRX achieves an output power of 7.9–8.9 dBm and an EVM of −25 dB with 8 $\times $ 100-MHz 5G NR frequency range 2 (FR2) orthogonal frequency division multiplexing (OFDM) 64-quadrature amplitude modulation (QAM) signals across 24–29.5 GHz, covering 3rd generation partnership project (3GPP) 5G NR FR2 operating bands (i.e., n257, n258, and n261) around 26 GHz. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is a common malignant tumor in the digestive system and a significant health burden worldwide. In this study, we found that hsa-let-7d-5p was upregulated in GC cells, promoted GC cell proliferation, migration, and invasion, and reduced apoptosis. Moreover, we found that the expression of PRDM5 (PR domain protein 5) was downregulated in GC cells and upregulated in GC cells treated with hsa-let-7d-5p inhibitor. Further investigation showed that hsa-let-7d-5p was the target of PRDM5, and the functions of hsa-let-7d-5p on GC progression were rescued by PRDM5 overexpression in GC cells. Collectively, our findings suggested that hsa-let-7d-5p promoted the development of GC by targeting PRDM5, indicating that hsa-let-7d-5p could be a promising therapeutic molecule for the treatment of gastric cancer. [ABSTRACT FROM AUTHOR]

A 1.9-dB NF K-band phased-array receiver (RX) is presented, which employs the hybrid packaged 65-nm CMOS beamformer and 0.1- $\mu \text{m}$ GaAs LNAs based on the fan-out wafer-level chip-scale packaging (WLCSP) technology. Power-efficient gain and phase tuning blocks are utilized to reduce power consumption. Temperature-healing design methodology is adopted to ensure nearly constant gain response versus temperature variations. The proposed phased-array RX only consumes 30.2-mW dc power per channel and achieves < 1.2-dB gain variation and < 0.9-dB NF variation from −40 °C to 85 °C. [ABSTRACT FROM AUTHOR]

With the proliferation of mobile devices and various sensors (e.g., GPS, magnetometer, accelerometers, gyroscopes) equipped, richer services, e.g. location based services, are provided to users. A series of methods have been proposed to protect the users’ privacy, especially the trajectory privacy. Hardware fingerprinting has been demonstrated to be a surprising and effective source for identifying/authenticating devices. In this work, we show that a few data samples collected from the motion sensors are enough to uniquely identify the source mobile device, i.e., the raw motion sensor data serves as a fingerprint of the mobile device. Specifically, we first analytically understand the fingerprinting capacity using features extracted from hardware data. To capture the essential device feature automatically, we design a multi-LSTM neural network to fingerprint mobile device sensor in real-life uses, instead of using handcrafted features by existing work. Using data collected over 6 months, for arbitrary user movements, our fingerprinting model achieves 93% F-score given one second data, while the state-of-the-art work achieves 79% F-score. Given ten seconds randomly sampled data, our model can achieve 98.8% accuracy. We also propose a novel generative model to modify the original sensor data and yield anonymized data with little fingerprint information while retain good data utility. [ABSTRACT FROM AUTHOR]

AbstractThis study systematically investigated the effect of position evolvement of four ribs in multicellular square tube on its crashworthiness performance. Results show that the multicellular square tubes with the shape factors of k = 0.25 and k = 0.75 have better energy absorption performances than other multicellular square tubes under the same wall thickness or the same mass. The mean crush force is derived through the simplified super folding element theory. Moreover, multi-objective optimization of multicellular square tube is carried out and the optimal result is validated by the finite element model. [ABSTRACT FROM AUTHOR]

Osteosarcoma (OS) is a primary malignant tumor of bone occurring in young adults. OS stem cells (OSCs) play an important role in the occurrence, growth, metastasis, drug resistance and recurrence of OS. CD133 is an integral membrane glycoprotein, which has been identified as an OSC marker. However, the mechanisms of metastasis, chemoresistance, and progression in CD133(+) OSCs need to be further explored. In this study, we aim to explore differences in miRNA levels between CD133(+) and CD133(-) cells from the MG-63 cell line. We found 20 differentially expressed miRNAs (DEmiRNAs) (16 upregulated and 4 downregulated) in CD133(+) cells compared with CD133(-) cells. Hsa-miR-4485-3p, hsa-miR-4284 and hsa-miR-3656 were the top three upregulated DEmiRNAs, while hsa-miR-487b-3p, hsa-miR-493-5p and hsa-miR-431-5p were the top three downregulated DEmiRNAs. In addition, RT-PCR analysis confirmed that the expression levels of hsa-miR-4284, hsa-miR-4485-3p and hsa-miR-3656 were significantly increased, while the expression levels of hsa-miR-487b-3p, hsa-miR-493-5p, and hsa-miR-431-5p were significantly decreased in CD133(+) cells compared with CD133(-) cells. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that predicted or validated target genes for all 20 DEmiRNAs or the selected 6 DEmiRNAs participated in the "PI3K-Akt signaling pathway," "Wnt signaling pathway," "Rap1 signaling pathway," "Cell cycle" and "MAPK signaling pathway". Among the selected six DEmiRNAs, miR-4284 was especially interesting. MiR-4284 knockdown significantly reduced the sphere forming capacity of CD133(+) OS cells. The number of invasive CD133(+) OS cells was markedly decreased after miR-4284 knockdown. In addition, miR-4284 knockdown increased the p-β-catenin levels in CD133(+) OS cells. In conclusion, RNA-seq analysis revealed DEmiRNAs between CD133(+) and CD133(-) cells. MiRNAs might play significant roles in the function of OSCs and could serve as targets for OS treatment. MiR-4284 prompted the self-renewal and invasion of OSCs. The function of miR-4284 might be associated with the Wnt signaling pathway., Competing Interests: The authors declare that they have no competing interests., (© 2021 Shu et al.)

Tumor endothelial cells have been found to be associated with metastasis and cancer progression. In this study, we reported that human esophageal cancer endothelial cells (HECEC), unlike corresponding human esophageal normal endothelial cells (HENEC) displayed several distinct feature couple with unique gene expression profile. Further studies showed that HECEC can enhance migration, invasion and self-renewal properties of esophageal carcinoma cell in vitro by a direct cell-cell interaction. In vivo assay demonstrated that HECEC could significantly enhance the invasion and lung metastasis of esophageal cancer cells. To elucidate the molecular mechanisms of HECEC in esophageal carcinoma progression, we employed the microarray to analyze the gene expression profiles before and after treating with HECEC, HENEC or conditioned meium from HECEC. Among the highly expressed HECEC-regulated genes, we focused on Epiregulin (EREG). Further studies demonstrated that overexpression of EREG in EC9706 or Kyse30 cells can induce actin reorganization, sphere formation ability and a significantly enrichment of CD44 + cancer stem-like cells. Moreover, up-regulation of EREG in esophageal cancer cells could enhance lung metastasis and decrease the survival time in vivo. Further study indicated that EREG could induce activation of the Src and FAK. In addition, all these effects could also be inhibited by the function-blocking anti-EREG antibody in a dose dependent manner. Immunohistochemical analysis revealed that high level of EREG was significantly correlated with lymph node metastases and poor prognosis. In summary, HECEC play key roles in enhancing the invasion, migration, cancer stem cell phenotype and metastatic potential of esophageal cancer cells through Epiregulin.