UniCat: Crafting a Stronger Fusion Baseline for Multimodal Re-Identification

Multimodal Re-Identification (ReID) is a popular retrieval task that aims to re-identify objects across diverse data streams, prompting many researchers to integrate multiple modalities into a unified representation. While such fusion promises a holistic view, our investigations shed light on potential pitfalls. We uncover that prevailing late-fusion techniques often produce suboptimal latent representations when compared to methods that train modalities in isolation. We argue that this effect is largely due to the inadvertent relaxation of the training objectives on individual modalities when using fusion, what others have termed modality laziness. We present a nuanced point-of-view that this relaxation can lead to certain modalities failing to fully harness available task-relevant information, and yet, offers a protective veil to noisy modalities, preventing them from overfitting to task-irrelevant data. Our findings also show that unimodal concatenation (UniCat) and other late-fusion ensembling of unimodal backbones, when paired with best-known training techniques, exceed the current state-of-the-art performance across several multimodal ReID benchmarks. By unveiling the double-edged sword of "modality laziness", we motivate future research in balancing local modality strengths with global representations.Comment: Accepted NeurIPS 2023 UniReps, 9 pages, 4 table

GraFT: Gradual Fusion Transformer for Multimodal Re-Identification

Object Re-Identification (ReID) is pivotal in computer vision, witnessing an escalating demand for adept multimodal representation learning. Current models, although promising, reveal scalability limitations with increasing modalities as they rely heavily on late fusion, which postpones the integration of specific modality insights. Addressing this, we introduce the \textbf{Gradual Fusion Transformer (GraFT)} for multimodal ReID. At its core, GraFT employs learnable fusion tokens that guide self-attention across encoders, adeptly capturing both modality-specific and object-specific features. Further bolstering its efficacy, we introduce a novel training paradigm combined with an augmented triplet loss, optimizing the ReID feature embedding space. We demonstrate these enhancements through extensive ablation studies and show that GraFT consistently surpasses established multimodal ReID benchmarks. Additionally, aiming for deployment versatility, we've integrated neural network pruning into GraFT, offering a balance between model size and performance.Comment: 3 Borderline Reviews at WACV, 8 pages, 5 figures, 8 table

Second generation androgen receptor antagonist, TQB3720 abrogates prostate cancer growth via AR/GPX4 axis activated ferroptosis

Purpose: Prostate cancer (PCa) poses a great threat to humans. The study aimed to evaluate the potential of TQB3720 in promoting ferroptosis to suppress prostate cancer, providing a theoretical basis for PCa therapy.Methods: PCa cells and nude mice models were divided into TQB3720, enzalutamide (ENZ), and control groups. Sulforhodamine B assay, colony formation assessment, organoids culture system, and the CCK8 assay were used for detecting proliferation. Western blot assay was processed to detect the expression of androgen receptor (AR), ferroptosis, and apoptosis-related genes. Flow cytometry was applied to measure the intracellular ROS levels. ELISA was performed to determine the cellular oxidized glutathione (GSSG) and malondialdehyde (MDA) levels. RT-qPCR was conducted to detect the mRNA expression of genes in AR signaling. BODIPYTM™ 581/591 was processed for detection of intracellular lipid peroxidation levels. The interaction of AR with other translational factor complex proteins was explored using Co-immunoprecipitation (Co-IP), and the chromatin immunoprecipitation (ChIP) assay was performed to detect the binding of AR-involved translational complex to downstream genes promoter. Luciferase reporter assay was conducted to examine the translation activity of GPX4 promoter, and immunohistochemistry (IHC) was conducted to analyze the levels of c-MYC, Ki-67 and AR in TQB3720-treated cancer tissues.Results: Here, we found TQB3720 inhibits the growth of prostate cancer in vitro and in vivo. TQB3720 treatment induced intracellular levels of GSSG and MDA significantly, by which hints AR antagonist caused ferroptosis-related cell death. Moreover, molecular evidence shown TQB3720 regulates downstream of AR signaling by binding AR resulting in inhibition of AR entry into the nucleus. Additional, we also proved that TQB3720 abrogates the interaction between AR and SP1 and leads to decrease GPX4 transcription.Conclusion: TQB3720 promotes ferroptosis in prostate cancer cells by reducing the AR/SP1 transcriptional complex binding to GPX4 promoter. As a result, it is suggested to be a potential drug for clinic prostate cancer treatment

Allosteric activation of the metabolic enzyme GPD1 inhibits bladder cancer growth via the lysoPC-PAFR-TRPV2 axis

Abstract Background Bladder cancer is the most common malignant tumor of the urinary system. Surgical resection and chemotherapy are the two mainstream treatments for bladder cancer. However, the outcomes are not satisfactory for patients with advanced bladder cancer. There is a need to further explore more effective targeted therapeutic strategies. Methods Proteomics were performed to compare protein expression differences between human bladder cancer tissues and adjacent normal tissues. The function of GPD1 on bladder cancer cells were confirmed through in vivo and in vitro assays. Transcriptomics and metabolomics were performed to reveal the underlying mechanisms of GPD1. Virtual screening was used to identify allosteric activator of GPD1. Results Here, we used proteomics to find that GPD1 expression was at low levels in bladder cancer tissues. Further investigation showed that GPD1 overexpression significantly promoted apoptosis in bladder cancer cells. Based on transcriptomics and metabolomics, GPD1 promotes Ca2+ influx and apoptosis of tumor cells via the lysoPC-PAFR-TRPV2 axis. Finally, we performed a virtual screening to obtain the GPD1 allosteric activator wedelolactone and demonstrated its ability to inhibit bladder tumor growth in vitro and in vivo. Conclusions This study suggests that GPD1 may act as a novel tumor suppressor in bladder cancer. Pharmacological activation of GPD1 is a potential therapeutic approach for bladder cancer

circCYP24A1 promotes Docetaxel resistance in prostate Cancer by Upregulating ALDH1A3

Abstract Background Docetaxel (DTX) is the most widely prescribed first-line chemotherapy for advanced prostate cancer (PCa). Unfortunately, DTX resistance invariably emerges, leading to worse prognosis of PCa. Growing evidence has shown that circRNAs had complex spatiotemporal specificity during the tumor development and oncogenesis. This study was designed to investigate the biological functions and possible molecular mechanisms of circRNAs in DTX resistance of PCa. Methods circRNAs in established DTX-resistant DU145 cell line were identified by RNA sequencing. Biological function of circCYP24A1 was verified in vitro and in vivo. The potential role of circCYP24A1 in the development of DTX-resistant PCa was investigated via dual-luciferase reporter assays, RIP assays and RNA pull-down assays. Univariate and multivariate logistic regression analyses was used to predict DTX-chemotherapy response based on patients’ clinical and biological information. Results CircCYP24A1 was identified to be upregulated in DTX-resistant DU145 cells. Upregulated circCYP24A1 was found to suppress the DTX chemosensitivity in vitro and in vivo. Furthermore, we found that circCYP24A1 promoted DTX resistance in PCa via regulating ALDH1A3 expression by sponging miR-1301-3p and activating PI3K/AKT/mTOR signaling pathway. Statistical analyses elucidated that circCYP24A1 was an independent risk factor to predict DTX response (OR = 0.165; 95% CI: 0.038–0.723; P = 0.017). Conclusions This study demonstrated that circCYP24A played an essential role in DTX resistance in PCa, suggesting that circCYP24A1 could be a promising biomarker to predict DTX response and a potential therapeutic target in PCa patients resistant to DTX chemotherapy

Differences of Typical Wuyi Rock Tea in Taste and Nonvolatiles Profile Revealed by Multisensory Analysis and LC–MS-Based Metabolomics

Wuyi Rock tea, specifically Shuixian and Rougui, exhibits distinct sensory characteristics. In this study, we investigated the sensory and metabolite differences between Shuixian and Rougui. Quantitative description analysis revealed that Rougui exhibited higher intensity in bitter, thick, harsh, and numb tastes, while Shuixian had stronger salty and umami tastes. Nontargeted metabolomics identified 151 compounds with 66 compounds identified as key differential metabolites responsible for metabolic discrimination. Most of the catechins and flavonoids were enriched in Rougui tea, while epigallocatechin-3,3′-di-O-gallate, epigallocatechin-3,5-di-O-gallate, gallocatechin-3,5-di-O-gallate, isovitexin, and theaflavanoside I were enriched in Shuixian tea. Catechins, kaempferol, quercetin, and myricetin derivatives were positively correlated with bitter taste and numb sensation. Sour taste was positively correlated to organic acids. Amino acids potentially contributed to salty and umami tastes. These results provide further insights into the taste characteristics and the relationship between taste attributes and specific metabolites in Wuyi Rock tea

Additional file 1 of Prediction of false-positive PI-RADS 5 lesions on prostate multiparametric MRI: development and internal validation of a clinical-radiological characteristics based nomogram

Supplementary Material