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A large number of objects of different scales appear aggregative distribution in remote sensing images, which brings two challenges to remote sensing object detection. The first challenge arises from the presence of objects with large scale differences within the same scene, which complicates the detector's ability to balance the detection performance between large and small objects. The second challenge is that the distribution of dense objects on remote sensing images with complex backgrounds can reduce the feature representation capability of the network, leading to false detections and missed detections of objects. To address the two challenges present in remote sensing object detection, we propose a new object detection network DA-GLANet (Direction-Aware Multi-Branch Attention and Gaussian Label Assignment Balance Net). For the first challenge, we designed a multi-scale feature fusion module to fully utilize semantic information at different scales, thereby improving the detection accuracy of multi-scale objects. Subsequently, to tackle the second challenge, we proposed a multi-branch attention module with direction-aware capabilities. This module can enhance the network's feature representation of objects of interest by generating attention maps that are both direction-aware and position-sensitive. In addition, we propose a label assignment strategy based on Gaussian distribution to address the imbalance of positive and negative labels caused by the complexity of remote sensing images. These methods work synergistically to improve aggregative object detection accuracy. We have conducted extensive experiments on the DOTA dataset, Levir dataset, and WHU buildings change detection dataset to demonstrate the superiority of our method. On the DOTA dataset, our method improves mAP by 0.4%, 0.3%, and 0.2% compared to the top three methods. On the Levir dataset, our method improves mAP by 2.5%, 2.2%, and 1.6% compared to the top three methods. [ABSTRACT FROM AUTHOR]

Background: Non‐apoptotic cell death is presently emerging as a potential direction to overcome the apoptosis resistance of cancer cells. In the current study, a natural plant agent α‐hederin (α‐hed) induces caspase‐independent paraptotic modes of cell death. Purpose: The present study is aimed to investigate the role of α‐hed induces paraptosis and the associated mechanism of it. Methods: The cell proliferation was detected by CCK‐8. The cytoplasm organelles were observed under electron microscope. Calcium (Ca2+) level was detected by flow cytometry. Swiss Target Prediction tool analyzed the potential molecule targets of α‐hed. Molecular docking methods were used to evaluate binding abilities of α‐hed with targets. The expressions of genes and proteins were analyzed by RT‐qPCR, western blotting, immunofluorescence, and immunohistochemistry. Xenograft models in nude mice were established to evaluate the anticancer effects in vivo. Results: α‐hed exerted significant cytotoxicity against a panel of CRC cell lines by inhibiting proliferation. Besides, it induced cytoplasmic vacuolation in all CRC cells. Electron microscopy images showed the aberrant dilation of endoplasmic reticulum and mitochondria. Both mRNA and protein expressions of Alg‐2 interacting proteinX (Alix), the marker of paraptosis, were inhibited by α‐hed. Besides, both Swiss prediction and molecular docking showed that the structure of α‐hed could tightly target to GPCRs. GPCRs were reported to activate the phospholipase C (PLC)‐β3/ inositol 1,4,5‐trisphosphate receptor (IP3R)/ Ca2+/ protein kinase C alpha (PKCα) pathway, and we then found all proteins and mRNA expressions of PLCβ3, IP3R, and PKCα were increased by α‐hed. After blocking the GPCR signaling, α‐hed could not elevate Ca2+ level and showed less CRC cell cytotoxicity. MAPK cascade is the symbol of paraptosis, and we then demonstrated that α‐hed activated MAPK cascade by elevating Ca2+ flux. Since non‐apoptotic cell death is presently emerging as a potential direction to overcome chemo‐drug resistance, we then found α‐hed also induced paraptosis in 5‐fluorouracil‐resistant (5‐FU‐R) CRC cells, and it reduced the growth of 5‐FU‐R CRC xenografts. Conclusions: Collectively, our findings proved α‐hed as a promising candidate for inducing non‐apoptotic cell death, paraptosis. It may overcome the resistance of apoptotic‐based chemo‐resistance in CRC. [ABSTRACT FROM AUTHOR]

Our team created the pathogenesis theory of cancer toxin in traditional Chinese medicine on the basis of inheriting the academic thought of "cancer toxins" of ZHOU Zhongying, a Chinese medical master.The pathogenesis theory of cancer toxin suggests that cancer toxins is the key factor leading to the occurrence and development of malignant tumors, the basic pathogenesis of malignant tumor is accumulation of evil and toxins, deficiency of vital qi. This paper proposes that the main pathological factors of carcinoma of prostate are deficiency, dampness, heat, stasis and toxins. The core pathogenesis was spleen and kidney deficiency, dampness-heat stasis toxin accumulation in essence chamber. The disease is located in the essence chamber, closely related to kidney and bladder, and involves liver and spleen. Clinical treatment is based on anti-cancer and detoxification, strengthening vital qi to eliminate pathogenic factor as the basic treatment principles, treatment with anti-cancer detoxification as the core, tonifying the spleen and kidney as the fundamental, clearing heat and removing dampness, removing blood stasis and dispersing is key, accompanied by dispersing liver and regulating qi, the whole syndrome differentiation, to maintain a stable period of time. Strengthening vital qi does not leave evil, eliminating evil does not harm vital qi. Guided by the pathogenesis theory of cancer toxin, this paper expounds the treatment of carcinoma of prostate based on syndrome differentiation and highlights the key role of the pathogenesis theory of cancer toxin in the treatment of this disease, providing reference for the differentiation and treatment of carcinoma of prostate. [ABSTRACT FROM AUTHOR]

Lung cancer is the most common type of cancer worldwide. Lung adenocarcinoma, a type of non-small cell lung cancer (NSCLC), is a common type of lung cancer. In recent years, immunotherapy has become the primary method of treatment for several solid cancers, including NSCLC. In the present study, the case of a patient with NSCLC following left superior lobectomy is reported. Different systemic therapies failed, such as a pemetrexed + carboplatin regimen, paclitaxel liposome + cisplatin and pembrolizumab, and albumin-bound paclitaxel + toripalimab, but long-term survival was achieved following targeted therapy and anti-programmed cell death protein-1 (PD-1) immunotherapy. The patient survived for >4 years following lung cancer progression, which is notably longer than expected for patients with advanced lung cancer. In conclusion, the present case demonstrated the efficacy of targeted therapy and anti-PD-1 immunotherapy for the treatment of advanced lung cancer following the occurrence of drug resistance and progressive disease. [ABSTRACT FROM AUTHOR]

Duodenal squamous cell carcinoma is an exceedingly rare occurrence among gastrointestinal malignancies, and its diagnosis and treatment are not well understood. In this report, we present a case of duodenal squamous cell carcinoma with liver and adrenal metastasis. The patient was treated with gemcitabine and S-1, achieving a progression-free survival (PFS) of 7 months and an overall survival (OS) of 9 months. Additionally, we review the features and treatment approaches reported in previous cases of primary duodenal carcinoma. Clearly, further case reports, such as ours, can contribute to a deeper understanding that is essential for characterizing this entity and establishing management guidelines., (S. Karger AG, Basel.)

Background: Colorectal cancer (CRC) is a malignancy with high incidence and mortality rates globally, categorized into left-sided and right-sided CRC, each exhibiting significant differences in molecular characteristics, clinical manifestations, and prognosis. Methods: This study employed single-cell transcriptomic data and various bioinformatics approaches, such as two-sample Mendelian randomization, reverse Mendelian randomization, colocalization analysis, directed filtering, pseudotime analysis, and intercellular communication analysis. It analyzed cellular-level disparities between left-sided and right-sided CRC, identifying distinct subpopulations with characteristic variations. For these cells, two-sample Mendelian randomization was utilized to explore gene-to-one-sided CRC causality. Results: LUCAT1 was enriched in high-abundance monocyte subpopulations in right-sided CRC and demonstrated potential risk factor status through Mendelian randomization analysis. The specific single-nucleotide polymorphism (SNP) rs10774624 was associated with an increased risk of CRC. Moreover, metabolic pathway analysis revealed that LUCAT1 + monocytes exhibit lower communication activity in the tumor microenvironment and heightened activity in metabolic functions like glycosaminoglycan degradation. Its biological functions are related to the positive regulation of interleukin-6 production and NF-kappa B signaling, among others. Conclusion: This study confirmed a potential causal relationship between LUCAT1 and right-sided CRC risk through Mendelian randomization analysis. These findings provide novel insights into the pathogenesis of right-sided CRC and may aid in developing early detection and treatment strategies for right-sided CRC., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Shang, Xi, Lai and Cheng.)

Background: Non-apoptotic cell death is presently emerging as a potential direction to overcome the apoptosis resistance of cancer cells. In the current study, a natural plant agent α-hederin (α-hed) induces caspase-independent paraptotic modes of cell death., Purpose: The present study is aimed to investigate the role of α-hed induces paraptosis and the associated mechanism of it., Methods: The cell proliferation was detected by CCK-8. The cytoplasm organelles were observed under electron microscope. Calcium (Ca 2+ ) level was detected by flow cytometry. Swiss Target Prediction tool analyzed the potential molecule targets of α-hed. Molecular docking methods were used to evaluate binding abilities of α-hed with targets. The expressions of genes and proteins were analyzed by RT-qPCR, western blotting, immunofluorescence, and immunohistochemistry. Xenograft models in nude mice were established to evaluate the anticancer effects in vivo., Results: α-hed exerted significant cytotoxicity against a panel of CRC cell lines by inhibiting proliferation. Besides, it induced cytoplasmic vacuolation in all CRC cells. Electron microscopy images showed the aberrant dilation of endoplasmic reticulum and mitochondria. Both mRNA and protein expressions of Alg-2 interacting proteinX (Alix), the marker of paraptosis, were inhibited by α-hed. Besides, both Swiss prediction and molecular docking showed that the structure of α-hed could tightly target to GPCRs. GPCRs were reported to activate the phospholipase C (PLC)-β3/ inositol 1,4,5-trisphosphate receptor (IP3R)/ Ca 2+ / protein kinase C alpha (PKCα) pathway, and we then found all proteins and mRNA expressions of PLCβ3, IP3R, and PKCα were increased by α-hed. After blocking the GPCR signaling, α-hed could not elevate Ca 2+ level and showed less CRC cell cytotoxicity. MAPK cascade is the symbol of paraptosis, and we then demonstrated that α-hed activated MAPK cascade by elevating Ca 2+ flux. Since non-apoptotic cell death is presently emerging as a potential direction to overcome chemo-drug resistance, we then found α-hed also induced paraptosis in 5-fluorouracil-resistant (5-FU-R) CRC cells, and it reduced the growth of 5-FU-R CRC xenografts., Conclusions: Collectively, our findings proved α-hed as a promising candidate for inducing non-apoptotic cell death, paraptosis. It may overcome the resistance of apoptotic-based chemo-resistance in CRC., (© 2024 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

Background: Colorectal cancer (CRC) ranks among the leading causes of cancerrelated deaths., Objective: This study aimed to illuminate the relationship between DPP7 (also known as DPP2) and CRC through a combination of bioinformatics and experimental methodologies., Methods: A multi-dimensional bioinformatic analysis on DPP7 was executed, covering its expression, survival implications, clinical associations, functional roles, immune interactions, and drug sensitivities. Experimental validations involved siRNA-mediated DPP7 knockdown and various cellular assays., Results: Data from the Cancer Genome Atlas (TCGA) identified high DPP7 expression in solid CRC tumors, with elevated levels adversely affecting patient prognosis. A shift from the N0 to the N2 stage in CRC was associated with increased DPP7 expression. Functional insights indicated the involvement of DPP7 in cancer progression, particularly in extracellular matrix disassembly. Immunological analyses showed its association with immunosuppressive entities, and in vitro experiments in CRC cell lines underscored its oncogenic attributes., Conclusion: DPP7 could serve as a CRC prognosis marker, functioning as an oncogene and representing a potential immunotherapeutic target., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)