Explore the vast range of titles available.

Compelling evidence has demonstrated the potential functions of circular RNAs (circRNAs) in breast cancer (BC) tumorigenesis. Nevertheless, the underlying mechanism by which circRNAs regulate BC progression is still unclear. The purpose of present research was to investigate the novel circRNA circRNF20 (hsa_circ_0087784) and its role in BC. CircRNA microarray sequencing revealed that circRNF20 was one of the upregulated transcripts in BC samples. Increased circRNF20 level predicted the poor clinical outcome in BC specimens. Functionally, circRNF20 promoted the proliferation and Warburg effect (aerobic glycolysis) of BC cells. Mechanistically, circRNF20 harbor miR-487a, acting as miRNA sponge, and then miR-487a targeted the 3'-UTR of hypoxia-inducible factor-1α (HIF-1α). Moreover, HIF-1α could bind with the promoter of hexokinase II (HK2) and promoted its transcription. In conclusion, this finding illustrates the vital roles of circRNF20 via the circRNF20/ miR-487a/HIF-1α/HK2 axis in breast cancer progress and Warburg effect, providing an interesting insight for the BC tumorigenesis.

Photovoltaic systems deployed on large floating platforms in nearshore waters are strongly influenced by hydroelastic effects, nonlinear shallow-water waves, and variable bathymetry. This study develops a time-domain hydroelastic framework that couples the fully nonlinear non-hydrostatic wave model NHWAVE with a Rankine-source potential-flow solver and a discrete-module Cummins formulation. The wave model provides incident pressures and kinematics over uneven seabeds, while the potential-flow solver evaluates radiation and diffraction effects and transfers the resulting hydrodynamic coefficients into the time domain. Numerical simulations are carried out for a 600 m modular floating structure under regular waves over flat and sloped bathymetries with tanα=0.0133, wave periods of 4–6 s, and wave heights of 0.3–1.0 m. The results show that bathymetric variation intensifies shoaling-induced excitation, modifies added-mass and damping distributions, increases the spatial non-uniformity of hydroelastic motions, and amplifies bending-moment RMS responses relative to the flat-bottom case. Additional comparisons between rigid-body and hydroelastic models show clear period-dependent redistribution of motions and bending demand. These results demonstrate that both local bathymetry and structural elasticity must be considered for the reliable analysis and design of nearshore floating photovoltaic systems and other large floating structures.

The wind direction is closely linked to the power performance and structural loads of wind turbines. Conventional nacelle‐mounted vanes or sonic anemometers face errors associated with airflow distortions caused by turbine blades. Nacelle‐mounted lidar systems offer line‐of‐sight speed measurements from multiple positions ahead of the rotor and rely on wind field reconstruction methods to predict the wind direction. This work considers three methods: the matrix inverse, the velocity azimuth display, and the physics‐informed neural network (PINN)–based methods. The first two are industrialized techniques that assume homogeneous flow. For flat terrain and offshore sites, the inhomogeneity of the mean flow is influenced by time‐averaging windows and turbine wakes. To illustrate the limitations and potential bias of wind direction estimates with homogeneous flow assumptions, we first present the bias using site measurement data. We then formulate a theoretical bias for a typical two‐beam lidar system. Next, we use openly available large eddy simulation data to evaluate the minute‐averaged wind direction estimates produced by the three methods. The first two methods are found to be unreliable, with maximum errors reaching close to 25° in the unwaked scenario and exceeding 30° in the waked case. As for the PINN‐based method, the errors remain within 10° across unwaked, waked, nonyawed, and yawed scenarios, even when only a 2D nonlinear convection equation is used as the physical constraint.

Scene text recognition (STR) is designed to automatically recognize the text content in natural scenes. Different from regular document text, text in natural scenes has the characteristics of irregular shapes, complex background, and distorted and blurred contents, which makes STR challenging. To solve the problems of STR for distorted, blurred, and low-resolution texts in natural scenes, this paper proposes a HRNet encoder and dual-branch decoder framework-based STR model. The model mainly consists of an encoder module and a dual-branch decoder module composed of a super-resolution branch and a recognition branch in parallel. In the encoder module, the HRNet is adopted to realize the cross-parallel aggregation representation with multiple resolutions during feature extraction and then outputs four kinds of feature maps with different resolutions. Moreover, the supervised attention module is used to strengthen the learning of the important feature information. In the decoder module, the dual-branch structure is adopted, in which the super-resolution branch takes the feature maps with the highest resolution obtained in the encoder module as input and restores images by upsampling through transposed convolution. The four kinds of feature maps with different resolutions are fused through independent transposed convolution layers for multiscale fusion in the recognition branch and then inputted into the attention-based decoder for text recognition. To improve the accuracy of text recognition, the feature extraction effect of the encoder module is together supervised by the super-resolution branch loss and the recognition branch loss. In addition, the super-resolution branch is only used for training and is abandoned during testing to reduce the complexity of the model. The proposed model is trained on Synth90K and SynthText datasets and tested on seven natural scene datasets. Compared with classical models such as ASTER, TextSR, and SCGAN, the recognition accuracy of the proposed model is improved and better recognition results can be achieved on irregular and blurred datasets such as IC15, SVTP, and CUTE80.

miR-34a is transcriptionally induced by the tumor suppressor gene p53, which is often downregulated in non-small cell lung cancer (NSCLC). To address whether the downstream signal of miR-34a is sufficient to induce apoptosis and to alter cellular radiosensitivity, a chemical synthetic miR-34a mimic was delivered into A549 and H1299 cells, with or without co-treatment of γ-irradiation. Results showed that ectopic expression of miR-34a induced dose-dependent cell growth inhibition and apoptosis in a p53-independent manner in both NSCLC cell lines. Interestingly, LyGDI was discovered as a new target gene of miR-34a, and downregulation of LyGDI promoted Rac1 activation and membrane translocation, resulting in cell apoptosis. Furthermore, restoration of miR-34a indirectly reduced cyclooxygenase-2 (COX-2) expression. Taken together, these results demonstrate that restoration of miR-34a expression enhances radiation-induced apoptosis, partly by suppressing the LyGDI signaling pathway, and miR-34a could possibly be used as a radiosensitizer for non-small cell lung cancer therapy.

ObjectiveThis study aimed to develop a personalized tantalum-based three-column porous screw (TTCPS) using selective laser melting technology to improve the osseointegration, mechanical stability, and biocompatibility of fracture fixation screws with porous architecture.MethodsTTCPS with an interconnected porous structure was customized through computer-aided design and fabricated using selective laser melting technique. Its mechanical properties were assessed via torsional resistance testing. Biocompatibility and osteogenic potential of TTCPS were evaluated on MC3T3-E1 cells by in vitro cell tests, including Live/Dead staining, scanning electron microscopy, alkaline phosphatase activity assays, and alizarin red staining. In vivo osseointegration capability of TTCPS was investigated using a comminuted fracture model in New Zealand white rabbits, with histological staining and mechanical pull-out tests that performed at 1, 2, and 3 months post-surgery.ResultsTTCPS demonstrated a torsional resistance of 2.83 ± 0.07 N·m, which is comparable to conventional high-strength titanium-based alloys (P > 0.05). In vitro experiments revealed high cell viability, pseudopod adhesion, and proliferation of MC3T3-E1 cells on TTCPS, alongside enhanced osteogenic differentiation and mineralization. In vivo studies showed progressive osseointegration, with pull-out forces of 123.6 ± 6.6 N, 370.6 ± 19.3 N, and 578.6 ± 21.3 N at 1, 2, and 3 months post-surgery, respectively.ConclusionWith its unique three-column structure, TTCPS improved primary stability and encouraged host bone ingrowth into its porous architecture, resulting in excellent osseointegration. This design overcomes clinical issues associated with traditional screws, such as screw fracture and bone defects. By integrating customized geometric optimization with biomimetic porous features, TTCPS provides a novel approach to fracture fixation, potentially transforming clinical management through enhanced biomechanical performance and biological integration.

Background Increasing evidence has indicated parathyroid hormone type 1 receptor (PTHR1) plays important roles for the development and progression of osteosarcoma (OS). However, its function mechanisms remain unclear. The goal of this study was to further illuminate the roles of PTHR1 in OS using microarray data. Methods Microarray data were available from the Gene Expression Omnibus database under the accession number GSE46861, including six tumors from mice with PTHR1 knockdown (PTHR1.358) and six tumors from mice with control knockdown (Ren.1309). Differentially expressed genes (DEGs) between PTHR1.358 and Ren.1309 were identified using the LIMMA method, and then, protein–protein interaction (PPI) network was constructed using data from STRING database to screen crucial genes associated with PTHR1. KEGG pathway enrichment analysis was performed to investigate the underlying functions of DEGs using DAVID tool. Results A total of 1163 genes were identified as DEGs, including 617 downregulated (Lef1, lymphoid enhancer-binding factor 1) and 546 upregulated genes (Dkk1, Dickkopf-related protein 1). KEGG enrichment analysis indicated upregulated DEGs were involved in Renin-angiotensin system (e.g., Agt, angiotensinogen) and Wnt signaling pathway (e.g., Dkk1), while downregulated DEGs participated in Basal cell carcinoma (e.g., Lef1). A PPI network (534 nodes and 2830 edges) was constructed, in which Agt gene was demonstrated to be the hub gene and its interactive genes (e.g., CCR3, CC chemokine receptor 3; and CCL9, chemokine CC chemokine ligand 9) were inflammation related. Conclusions Our present study preliminarily reveals the pro-malignant effects of PTHR1 in OS cells may be mediated by activating Wnt, angiogenesis, and inflammation pathways via changing the expressions of the crucial enriched genes (Dkk1, Lef1, Agt-CCR3, and Agt-CCL9).

Compelling evidence has demonstrated the potential functions of circular RNAs (circRNAs) in breast cancer (BC) tumorigenesis. Nevertheless, the underlying mechanism by which circRNAs regulate BC progression is still unclear. The purpose of present research was to investigate the novel circRNA circRNF20 (hsa_circ_0087784) and its role in BC. CircRNA microarray sequencing revealed that circRNF20 was one of the upregulated transcripts in BC samples. Increased circRNF20 level predicted the poor clinical outcome in BC specimens. Functionally, circRNF20 promoted the proliferation and Warburg effect (aerobic glycolysis) of BC cells. Mechanistically, circRNF20 harbor miR-487a, acting as miRNA sponge, and then miR-487a targeted the 3’-UTR of hypoxia-inducible factor-1α (HIF-1α). Moreover, HIF-1α could bind with the promoter of hexokinase II (HK2) and promoted its transcription. In conclusion, this finding illustrates the vital roles of circRNF20 via the circRNF20/ miR-487a/HIF-1α/HK2 axis in breast cancer progress and Warburg effect, providing an interesting insight for the BC tumorigenesis.

This study aimed to determine the interactions between parathyroid hormone type 1 receptor (PTHR1) and angiotensinogen (AGT) and the effects of these agents on osteosarcoma (OS). We constructed a stably transfected mouse OS K7M2 cell line (shPTHR1‐ K7M2) using shRNA and knocked down AGT in these cells using siRNA‐AGT. The transfection efficiency and expression of AGT, chemokine C‐C motif receptor 3 (CCR3), and chemokine (C‐C motif) ligand 9 (CCL9) were determined using real‐time quantitative PCR. Cell viability and colony formation were assessed using Cell Counting Kit‐8 and crystal violet staining, respectively. Cell apoptosis and cycle phases were assessed by flow cytometry, and cell migration and invasion were evaluated using Transwell assays. Interference with PTHR1 upregulated the expression of AGT and CCR3, and downregulated that of CCL9, which was further downregulated by AGT knockdown. Cell viability, migration, invasion and colony formation were significantly decreased, while cell apoptosis was significantly increased in shPTHR1‐K7M2, compared with those in K7M2 cells (P < .05 for all). However, AGT knockdown further inhibited cell viability after 72 h of culture but promoted cell migration and invasion. PTHR1 interference decreased and increased the numbers of cells in the G0/G1 and G2/M phases, respectively, compared with those in K7M2 cells. Angiotensinogen knockdown increased the number of cells in the G0/G1 phase compared with that in the shPTHR1‐K7M2 cells. Therefore, PTHR1 affects cell viability, apoptosis, migration, invasion and colony formation, possibly by regulating AGT/CCL9 in OS cells.