41 research outputs found

    3D-STMN: Dependency-Driven Superpoint-Text Matching Network for End-to-End 3D Referring Expression Segmentation

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    In 3D Referring Expression Segmentation (3D-RES), the earlier approach adopts a two-stage paradigm, extracting segmentation proposals and then matching them with referring expressions. However, this conventional paradigm encounters significant challenges, most notably in terms of the generation of lackluster initial proposals and a pronounced deceleration in inference speed. Recognizing these limitations, we introduce an innovative end-to-end Superpoint-Text Matching Network (3D-STMN) that is enriched by dependency-driven insights. One of the keystones of our model is the Superpoint-Text Matching (STM) mechanism. Unlike traditional methods that navigate through instance proposals, STM directly correlates linguistic indications with their respective superpoints, clusters of semantically related points. This architectural decision empowers our model to efficiently harness cross-modal semantic relationships, primarily leveraging densely annotated superpoint-text pairs, as opposed to the more sparse instance-text pairs. In pursuit of enhancing the role of text in guiding the segmentation process, we further incorporate the Dependency-Driven Interaction (DDI) module to deepen the network's semantic comprehension of referring expressions. Using the dependency trees as a beacon, this module discerns the intricate relationships between primary terms and their associated descriptors in expressions, thereby elevating both the localization and segmentation capacities of our model. Comprehensive experiments on the ScanRefer benchmark reveal that our model not only set new performance standards, registering an mIoU gain of 11.7 points but also achieve a staggering enhancement in inference speed, surpassing traditional methods by 95.7 times. The code and models are available at https://github.com/sosppxo/3D-STMN

    Spatiotemporal Evolution and Influencing Factors of Ecological Civilization Construction in China

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    The construction of an ecological civilization is a strategic idea proposed based on the conditions of different countries and the laws governing social development. It is a new way to promote harmonious coexistence between humans and nature. Therefore, exploring the evolution characteristics and influence of ecological civilization in China is helpful for the country’s future development. This study uses the pentagon model, panel threshold regression model, and spatial analysis tool to explore the law of space-time differentiation and analyze regional coordination and ecological civilization construction in 31 provinces, cities, and autonomous regions in China from 2000 to 2018. During the study period, the construction of ecological civilization in China generally fluctuated; the spatial differentiation pattern of the eastern region was more developed than that of the central region, which was more developed than that of the western region. The regional coordination degree decreased in the order of east >central >northeast >west, and the degree of coordination in provinces and cities gradually shifted and finally accumulated to be reflected in the economy and environment in 2018. The most important factor affecting the development of ecological civilization was determined to be scientific research, followed by air quality and government information disclosure

    LDPC Codes Based on the Space of Symmetric Matrices Over Finite Fields

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    Fluidized Bed Agglomeration Diagnosis Based on Wavelet Packet Entropy and Gaussian Test

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    Aiming at the synthesis process through the ethylene polymerization by virtue of fluidized bed reactors, this paper proposed a different approach for agglomeration monitoring and early alarming in polymerization reaction with Gaussian test of wavelet packet entropies from low-frequency audible acoustic signals. In comparison to high-frequency acoustic emission signals, audible acoustic signals can reduce the signal bandwidth, simplify the signal processing circuit, facilitate the real-time measurement, and fault detection. Compared with the approach based on regression modeling and pattern recognition, this approach can overcome the defects of false alarm and missing alarm caused by inadequate samples and weak generalization capability of diagnosis model and is easy to be implemented. Experiments in a pilot plant have verified the effectiveness of the approach, and earlier warning could be realized compared with the existing approaches on the production apparatus (material level detection and temperature measurement)

    BAP31 Promotes Angiogenesis via Galectin-3 Upregulation in Neuroblastoma

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    Neuroblastoma (NB) is one of the highly vascularized childhood solid tumors, and understanding the molecular mechanisms underlying angiogenesis in NB is crucial for developing effective therapeutic strategies. B-cell receptor-associated protein 31 (BAP31) has been implicated in tumor progression, but its role in angiogenesis remains unexplored. This study investigated BAP31 modulation of pro-angiogenic factors in SH-SY5Y NB cells. Through protein overexpression, knockdown, antibody blocking, and quantification experiments, we demonstrated that overexpression of BAP31 led to increased levels of vascular endothelial growth factor A (VEGFA) and Galectin-3 (GAL-3), which are known to promote angiogenesis. Conditioned medium derived from BAP31-overexpressing neuroblastoma cells stimulated migration and tube formation in endothelial cells, indicating its pro-angiogenic properties. Also, we demonstrated that BAP31 enhances capillary tube formation by regulating hypoxia-inducible factor 1 alpha (HIF-1α) and its downstream target, GAL-3. Furthermore, GAL-3 downstream proteins, Jagged 1 and VEGF receptor 2 (VEGFR2), were up-regulated, and blocking GAL-3 partially inhibited the BAP31-induced tube formation. These findings suggest that BAP31 promotes angiogenesis in NB by modulating GAL-3 and VEGF signaling, thereby shaping the tumor microenvironment. This study provides novel insights into the pro-angiogenic role of BAP31 in NB

    Knockdown of BAP31 Overcomes Hepatocellular Carcinoma Doxorubicin Resistance through Downregulation of Survivin

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    The expression of B-cell receptor associated protein 31 (BAP31) is increased in many tumor types, and it is reported to participate in proliferation, migration, and apoptosis. However, the relationship between BAP31 and chemoresistance is uncertain. This study investigated the role of BAP31 in regulating the doxorubicin (Dox) resistance of hepatocellular carcinoma (HCC). The expression of proteins was assessed by Western blotting. The correlation between BAP31 expression and Dox resistance was examined by MTT and colony formation assays. Apoptosis was analyzed by flow cytometry and TdT-mediated dUTP nick end labeling assays. Western blot and immunofluorescence analyses were performed in the knockdown cell lines to explore the possible mechanisms. In this study, BAP31 was strongly expressed, and knockdown of BAP31 increased Dox chemosensitivity in cancer cells. Furthermore, the expression of BAP31 was higher in the Dox-resistant HCC cells than that in their parental cells; knockdown of BAP31 reduced the half maximal inhibitory concentration value and overcame Dox resistance in Dox-resistant HCC cells. In HCC cells, knockdown of BAP31 increased Dox-induced apoptosis and enhanced Dox chemosensitivity in vitro and in vivo. The potential mechanism by which BAP31 increased Dox-induced apoptosis is that BAP31 inhibited survivin expression by promoting FoxO1 nucleus–cytoplasm translocation. Knockdown of BAP31 and survivin had a synergistic effect on Dox chemosensitivity by enhancing the apoptosis of HCC cells. These findings reveal that BAP31 knockdown enhances Dox chemosensitivity through the downregulation of survivin, suggesting that BAP31 is a potential therapeutic target for improving the treatment response of HCC with resistance to Dox

    Knockdown of BAP31 Downregulates Galectin-3 to Inhibit the Wnt/β-Catenin Signaling Pathway to Modulate 5-FU Chemosensitivity and Cancer Stemness in Colorectal Cancer

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    Increased stemness is causally linked to the development of chemoresistance in cancers. B-cell receptor-associated protein 31 (BAP31) has been identified to play an oncogenic role in many types of cancer. However, the role of BAP31 in 5-fluorouracil (5-FU) chemosensitivity and stemness of colorectal cancer (CRC) is still unknown. The aim of this study was to investigate the biological function and molecular mechanism of BAP31 in regulating 5-FU chemosensitivity and stemness. The correlation between BAP31 expression and 5-FU chemosensitivity was examined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and colony formation assays. Cancer stemness was analyzed using tumor sphere formation and Western blot assays. Western blot and immunofluorescence analyses of the knockdown cell lines were performed to explore the possible mechanisms. Finally, we investigated the function of BAP31 by constructing xenograft nude mouse models in vivo. In this study, we demonstrated that BAP31 was increased in CRC cells, and knockdown of BAP31 reduced the half maximal inhibitory concentration (IC50) of 5-FU, while this effect was reversed by overexpression of BAP31. In addition, knockdown of BAP31 substantially reduced the stemness of CRC cells in vitro. Consistently, knockdown of BAP31 significantly suppressed the tumorigenicity and stemness of CRC in vivo. The functional study further suggested that knockdown of BAP31 downregulated galectin-3 to inhibit the accumulation of β-catenin, which in turn repressed the transcription of downstream target genes (c-MYC, SOX2) of the Wnt/β-catenin signaling pathway. Knockdown of BAP31 reduced stemness by inhibiting the Wnt/β-catenin signaling pathway to increase 5-FU chemosensitivity. Importantly, intrabodies against BAP31 suppressed tumor growth and enhanced the antitumor effects of 5-FU in vivo. Therefore, using intrabodies against BAP31 may be a strategy for improving the antitumor effect of 5-FU in CRC
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