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867 result(s) for "Zhang Pengpeng"
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HAMD-DETR: A Wind Turbine Defect Detection Method Integrating Multi-Scale Feature Perception
Wind turbines operating in harsh environments are prone to surface defects that compromise efficiency and safety. Traditional convolutional neural networks lack sufficient multi-scale feature representation, while Transformer-based methods suffer from excessive computational complexity. This study proposes HAMD-DETR, an end-to-end detection framework for wind turbine defect identification. The framework consists of three key components: an Adaptive Dynamic Multi-scale Perception Network (ADMPNet), a Hierarchical Dynamic Feature Pyramid Network (HDFPN), and a Dynamic Frequency-Domain Feature Encoder (DFDEncoder). Firstly, ADMPNet integrates multi-scale dynamic integration fusion and adaptive inception depthwise convolution for feature extraction. Then the HDFPN balances deep semantic and shallow detail features through pyramid adaptive context extraction and gradient refinement modules. At last, DFDEncoder enhances feature discrimination through frequency-domain transformation. Experiments on wind turbine datasets demonstrate that HAMD-DETR achieves 58.6% mAP50 and 31.7% mAP50-95, representing improvements of 3.1% and 2.1% over the baseline RT-DETR. The proposed method reduces computational complexity by 27.2% and parameters by 30% while achieving a 151.9 FPS inference speed. These results validate HAMD-DETR’s effectiveness for wind turbine defect detection and demonstrate its potential for intelligent operation and maintenance applications.
Leveraging mitochondrial-programmed cell death dynamics to enhance prognostic accuracy and immunotherapy efficacy in lung adenocarcinoma
BackgroundLung adenocarcinoma (LUAD) is a highly heterogeneous disease, posing significant challenges to accurate prognosis prediction. Mitochondria play a central role in the energy metabolism of eukaryotic cells and can influence programmed cell death (PCD) mechanisms, which are critical in tumorigenesis and cancer progression. However, the prognostic significance of the interplay between mitochondrial function and PCD in LUAD requires further investigation.MethodsWe analyzed data from 1231 LUAD patients across seven global cohorts to develop a mitochondrial-related PCD signature (MPCDS) using machine learning. Validation was done using six immunotherapy cohorts (LUAD, melanoma, clear cell renal cell carcinoma; n=935) and a pan-cancer cohort of 21 tumor types. An in-house LUAD tissue cohort (n=100) confirmed the prognostic significance of nucleoside diphosphate kinase 4 (NME4). In vivo and in vitro experiments explored NME4’s role in immune exclusion.ResultsThe MPCDS demonstrated strong predictive performance for prognosis in LUAD patients, surpassing 114 previously published LUAD signatures. Additionally, MPCDS effectively predicted outcomes in immunotherapy patients (including those with LUAD, melanoma, and clear cell renal cell carcinoma). Biologically, MPCDS was significantly associated with immune features, with the high MPCDS group exhibiting reduced immune activity and a tendency towards cold tumors. NME4, a key gene within the MPCDS (correlation=0.55, p<0.05), was associated with poorer prognosis in LUAD patients with high expression, particularly in CD8 desert phenotypes, as validated by our in-house cohort. Multiplex immunofluorescence confirmed the spatial colocalization and exclusion relationship between NME4 and immune cells such as CD3+ T cells and CD20+ B cells. Further experiments revealed that NME4 regulated the proliferation and invasion of LUAD cells both in vitro and in vivo. Importantly, inhibiting NME4 increased the abundance and activity of CD8+ T cells and enhanced the antitumor immunity of anti-programmed cell death protein-1 therapy in vivo.ConclusionThe MPCDS provides personalized risk assessment and immunotherapy interventions for individual LUAD patients. NME4, a key gene within the MPCDS, has been identified as a novel oncogene associated with immune exclusion and may serve as a new target for LUAD intervention and immunotherapy.
The influence of the brand image of green agriculture products on China’s consumption intention——The mediating role of perceived value
Green agriculture can minimize the negative impact of agriculture on the environment. As countries around the world strongly advocate green production and green life style, not only is consumers’ awareness about green consumption rising, but the demand for green agricultural products at home and abroad is gradually increasing as well. Brand image has been a crucial factor for consumers to make their final purchasing decisions, thus playing a critical role in influencing the purchasing decisions of consumers. Based on the theory of the brand image, this paper undergoes a comprehensive theoretical and positive analysis and explores the influence mechanism of brand image of green agricultural products on consumers’ purchasing intention. A hypothetical model with perceived value as mediators is constructed by us to examine the influence of brand image of green agricultural products on consumers’ purchasing intention. A quantitative study was conducted for a random sample of 341 consumers who purchased green agricultural products in China according to a questionnaire-based survey using a cluster random sampling technique. The study showed that the overall image of agribusiness, the image of agricultural products, the social image of agribusiness, and the image of consumers are all positively related to consumption intention. The overall image of agribusiness, the image of agricultural products, the social image of agribusiness, and the image of consumers have a positive influence on perceived value. Moreover, perceived value plays a part in the mediating role in the influence of the overall image of agribusiness, the image of agricultural products, the social image of agribusiness, and the image of consumers on consumption intention. These findings shed lights on enterprises in establishing a scientific and effective brand strategy and building an excellent brand image. The research conclusion can provide new insight into how to enhance the consumption willingness for green agricultural products and promote sustainable development.
Novel post-translational modification learning signature reveals B4GALT2 as an immune exclusion regulator in lung adenocarcinoma
BackgroundLung adenocarcinoma (LUAD) presents significant challenges in prognosis and treatment efficacy evaluation. While post-translational modifications are known to influence tumor progression, their prognostic value in LUAD remains largely unexplored.MethodsWe developed a post-translational modification learning signature (PTMLS) using machine learning techniques, analyzing data from 1231 LUAD patients across seven global cohorts. The signature’s efficacy in predicting immunotherapy response was evaluated using 12 immunotherapy cohorts spanning multiple cancer types (n=1201). An in-house LUAD tissue cohort (n=171) was used to validate beta-1,4-galactosyltransferase 2’s (B4GALT2’s) prognostic significance. The role of B4GALT2 in immune exclusion was investigated through in vivo and in vitro experiments.ResultsThe established PTMLS exhibited exceptional predictive capabilities in LUAD patient outcomes, surpassing the efficacy of 98 existing LUAD prognostic indicators. The system’s predictive value was validated across diverse malignancy categories for immunotherapeutic response assessment. From a biological perspective, significant correlations were observed between PTMLS and immunological parameters, whereby elevated PTMLS levels were characterized by attenuated immune responses and immunologically cold neoplastic features. Within the PTMLS framework, B4GALT2 was identified as a crucial molecular component (r=0.82, p<0.05), and its heightened expression was linked to unfavorable clinical outcomes in LUAD cases, particularly in specimens exhibiting CD8-depleted phenotypes. The spatial distribution patterns between B4GALT2 and immune cell populations, specifically CD8+ T lymphocytes and CD20+ B lymphocytes, were elucidated through multiplexed immunofluorescence analysis. Laboratory investigations subsequently established B4GALT2’s regulatory influence on LUAD cellular expansion in both laboratory cultures and animal models. Significantly, suppression of B4GALT2 was found to enhance CD8+ T lymphocyte populations and their functional status, thereby potentiating anti-programmed cell death protein 1 immunotherapeutic efficacy in animal studies. This phenomenon was characterized by reduced CD62L+CD8 T lymphocyte levels alongside elevated GZMB+/CD44+/CD69+CD8 T cell populations.ConclusionThe developed PTMLS system represents an effective instrument for individualized prognostic evaluation and immunotherapy stratification in both LUAD and diverse cancer populations. The identification of B4GALT2 as a previously unrecognized oncogenic factor involved in immune exclusion presents a novel therapeutic avenue for LUAD treatment and immunotherapy optimization.
Unraveling molecular networks in thymic epithelial tumors: deciphering the unique signatures
Thymic epithelial tumors (TETs) are a rare and diverse group of neoplasms characterized by distinct molecular signatures. This review delves into the complex molecular networks of TETs, highlighting key aspects such as chromosomal abnormalities, molecular subtypes, aberrant gene mutations and expressions, structural gene rearrangements, and epigenetic changes. Additionally, the influence of the dynamic tumor microenvironment on TET behavior and therapeutic responses is examined. A thorough understanding of these facets elucidates TET pathogenesis, offering avenues for enhancing diagnostic accuracy, refining prognostic assessments, and tailoring targeted therapeutic strategies. Our review underscores the importance of deciphering TETs’ unique molecular signatures to advance personalized treatment paradigms and improve patient outcomes. We also discuss future research directions and anticipated challenges in this intriguing field.
Mitochondrial Pathway Signature (MitoPS) predicts immunotherapy response and reveals NDUFB10 as a key immune regulator in lung adenocarcinoma
BackgroundLung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer. Although immune checkpoint inhibitors (ICIs) have brought new treatment options for advanced patients, a considerable proportion still shows limited response. Mitochondrial dysfunction plays a crucial role in tumor development and immune evasion, but its regulatory mechanisms in LUAD immune microenvironment remain unclear.MethodsWe integrated 149 mitochondria-related pathways (1,136 coding proteins) to develop and validate the Mitochondrial Pathway Signature (MitoPS) using machine learning approaches across seven independent LUAD cohorts (n=1,231). The system was systematically compared with 129 published LUAD prognostic signatures and validated in seven immunotherapy cohorts (n=451). Multiomics analysis, immunofluorescence staining, and experimental validation were performed to investigate its molecular mechanism.ResultsMitoPS demonstrated consistent predictive performance across validation cohorts, with high scores indicating poor prognosis, outperforming 129 existing prognostic models. In immunotherapy cohorts, MitoPS reliably predicted treatment response and prognosis. Immune microenvironment analysis revealed that low MitoPS scores correlated with higher immune cell infiltration and active immune function. Mechanistic studies identified mitochondria-related gene NDUFB10 as a core gene of MitoPS (r=0.38, p<0.05), where its high expression was significantly associated with immune desert phenotype and worse prognosis. Functional experiments confirmed that NDUFB10 knockdown significantly enhanced ICIs therapy and increased GZMB+CD8+T cell infiltration, indicating NDUFB10’s crucial role in regulating tumor immune microenvironment and immunotherapy response.ConclusionThe MitoPS scoring system reliably predicts prognosis and immunotherapy response in patients with LUAD, providing a novel reference for clinical decision-making. Furthermore, its core gene NDUFB10 regulates tumor immune microenvironment, offering a potential therapeutic target for improving immunotherapy outcomes.
A novel signature predicts prognosis and immunotherapy in lung adenocarcinoma based on cancer-associated fibroblasts
Extensive research has established the significant correlations between cancer-associated fibroblasts (CAFs) and various stages of cancer development, including initiation, angiogenesis, progression, and resistance to therapy. In this study, we aimed to investigate the characteristics of CAFs in lung adenocarcinoma (LUAD) and develop a risk signature to predict the prognosis of patients with LUAD. We obtained single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data from the public database. The Seurat R package was used to process the scRNA-seq data and identify CAF clusters based on several biomarkers. CAF-related prognostic genes were further identified using univariate Cox regression analysis. To reduce the number of genes, Lasso regression was performed, and a risk signature was established. A novel nomogram that incorporated the risk signature and clinicopathological features was developed to predict the clinical applicability of the model. Additionally, we conducted immune landscape and immunotherapy responsiveness analyses. Finally, we performed experiments to verify the functions of EXO1 in LUAD. We identified 5 CAF clusters in LUAD using scRNA-seq data, of which 3 clusters were significantly associated with prognosis in LUAD. A total of 492 genes were found to be significantly linked to CAF clusters from 1731 DEGs and were used to construct a risk signature. Moreover, our immune landscape exploration revealed that the risk signature was significantly related to immune scores, and its ability to predict responsiveness to immunotherapy was confirmed. Furthermore, a novel nomogram incorporating the risk signature and clinicopathological features showed excellent clinical applicability. Finally, we verified the functions of EXP1 in LUAD through experiments. The risk signature has proven to be an excellent predictor of LUAD prognosis, stratifying patients more appropriately and precisely predicting immunotherapy responsiveness. The comprehensive characterization of LUAD based on the CAF signature can predict the response of LUAD to immunotherapy, thus offering fresh perspectives into the management of LUAD patients. Our study ultimately confirms the role of EXP1 in facilitating the invasion and growth of tumor cells in LUAD. Nevertheless, further validation can be achieved by conducting experiments.
B4GALT1 promotes immune escape by regulating the expression of PD-L1 at multiple levels in lung adenocarcinoma
Background Invasive adenocarcinoma (IAC), which is typically preceded by minimally invasive adenocarcinoma (MIA), is the dominant pathological subtype of early-stage lung adenocarcinoma (LUAD). Identifying the molecular events underlying the progression from MIA to IAC may provide a crucial perspective and boost the exploration of novel strategies for early-stage LUAD diagnosis and treatment. Methods Transcriptome sequencing of four pairs of MIA and IAC tumours obtained from four multiple primary lung cancer patients was performed to screen out beta-1,4-galactosyltransferase1 ( B4GALT1 ). Function and mechanism experiments in vitro and in vivo were performed to explore the regulatory mechanism of B4GALT1 -mediated immune evasion by regulating programmed cell death ligand 1 (PD-L1). Results B4GALT1 , a key gene involved in N-glycan biosynthesis, was highly expressed in IAC samples. Further experiments revealed that B4GALT1 regulated LUAD cell proliferation and invasion both in vitro and in vivo and was related to the impaired antitumour capacity of CD8 + T cells. Mechanistically, B4GALT1 directly mediates the N-linked glycosylation of PD-L1 protein, thus preventing PD-L1 degradation at the posttranscriptional level. In addition, B4GALT1 stabilized the TAZ protein via glycosylation, which activated CD274 at the transcriptional level. These factors lead to lung cancer immune escape. Importantly, inhibition of B4GALT1 increased CD8 + T-cell abundance and activity and enhanced the antitumour immunity of anti-PD-1 therapy in vivo. Conclusion B4GALT1 is a critical molecule in the development of early-stage LUAD and may be a novel target for LUAD intervention and immunotherapy.
By integrating single-cell RNA-seq and bulk RNA-seq in sphingolipid metabolism, CACYBP was identified as a potential therapeutic target in lung adenocarcinoma
Lung adenocarcinoma (LUAD) is a heterogeneous disease with a dismal prognosis for advanced tumors. Immune-associated cells in the microenvironment substantially impact LUAD formation and progression, which has gained increased attention in recent decades. Sphingolipids have a profound impact on tumor formation and immune infiltration. However, few researchers have focused on the utilization of sphingolipid variables in the prediction of LUAD prognosis. The goal of this work was to identify the major sphingolipid-related genes (SRGs) in LUAD and develop a valid prognostic model based on SRGs. The most significant genes for sphingolipid metabolism (SM) were identified using the AUCell and WGCNA algorithms in conjunction with single-cell and bulk RNA-seq. LASSO and COX regression analysis was used to develop risk models, and patients were divided into high-and low-risk categories. External nine provided cohorts evaluated the correctness of the models. Differences in immune infiltration, mutation landscape, pathway enrichment, immune checkpoint expression, and immunotherapy were also further investigated in distinct subgroups. Finally, cell function assay was used to verify the role of CACYBP in LUAD cells. A total of 334 genes were selected as being most linked with SM activity for further investigation, and a risk model consisting of 11 genes was established using lasso and cox regression. According to the median risk value, patients were split into high- and low-risk groups, and the high-risk group had a worse prognosis. The low-risk group had more immune cell infiltration and higher expression of immune checkpoints, which illustrated that the low-risk group was more likely to benefit from immunotherapy. It was verified that CACYBP could increase the ability of LUAD cells to proliferate, invade, and migrate. The eleven-gene signature identified in this research may help physicians create individualized care plans for LUAD patients. CACYBP may be a new therapeutic target for patients with advanced LUAD.
Forked-Crossing Metasurface for Multi-Band Polarization Conversion with Distinct Bandwidths
This study presents a reflective and highly efficient multi-band metasurface polarization converter based on a forked-crossing patch array. Both simulation and experimental results reveal that such a metasurface achieves polarization conversion ratio (PCR) exceeding 90% over five frequency bands of 4.71–5.44 GHz, 7.26–9.55 GHz, 11.62–12.6 GHz, 13.33–13.46 GHz, and 15.61–15.62 GHz with high conversion efficiency realized at five distinct resonances. The quality-factor (Q-factor) analysis of each band reveals a hybrid behavior. More specifically, the first and second bands exhibit relatively low Q factors of approximately 6.95 and 3.67, indicating wideband polarization conversion capability. The third band has a moderate Q factor of 12.35, while the fourth and fifth bands show high-Q resonances with Q factors of 103.04 and 1561.5, respectively, indicating sharp and selective frequency responses. This combination of wideband and high-Q narrowband responses makes the proposed design especially suitable for complex electromagnetic scenarios, such as multifunctional radar, communication, and sensing systems, where both broad frequency coverage and precise spectral control are simultaneously required.