116 research outputs found
An Empirical Study of Low-carbon Lifestyle
This paper mainly organizes the theory of lifestylefrom the fields of sociology and consumer behavior, it alsooutlines the situation of domestic scholars on the study of thelow-carbon lifestyle. Then this paper does an empiricalresearch, with the method of structural equation, onlow-carbon lifestyle in which residents of Dalian are theobjects of study. And it defines low-carbon lifestyle as asustainable way of life which includes low-carbon publicbehavior, daily low-carbon behavior, social behavior,environmental attitude and low-carbon acknowledgment. Thispaper also finds out that the environmental attitude andlow-carbon acknowledgment affect peopleās low-carbonbehavior, includes low-carbon public behavior, social behaviorand daily low0carbon behavior. In the end of the paper, it putsforward the limitations of this study as well as a researchdirection for lifestyle in the future
Efficient Teacher: Semi-Supervised Object Detection for YOLOv5
Semi-Supervised Object Detection (SSOD) has been successful in improving the
performance of both R-CNN series and anchor-free detectors. However, one-stage
anchor-based detectors lack the structure to generate high-quality or flexible
pseudo labels, leading to serious inconsistency problems in SSOD. In this
paper, we propose the Efficient Teacher framework for scalable and effective
one-stage anchor-based SSOD training, consisting of Dense Detector, Pseudo
Label Assigner, and Epoch Adaptor. Dense Detector is a baseline model that
extends RetinaNet with dense sampling techniques inspired by YOLOv5. The
Efficient Teacher framework introduces a novel pseudo label assignment
mechanism, named Pseudo Label Assigner, which makes more refined use of pseudo
labels from Dense Detector. Epoch Adaptor is a method that enables a stable and
efficient end-to-end semi-supervised training schedule for Dense Detector. The
Pseudo Label Assigner prevents the occurrence of bias caused by a large number
of low-quality pseudo labels that may interfere with the Dense Detector during
the student-teacher mutual learning mechanism, and the Epoch Adaptor utilizes
domain and distribution adaptation to allow Dense Detector to learn globally
distributed consistent features, making the training independent of the
proportion of labeled data. Our experiments show that the Efficient Teacher
framework achieves state-of-the-art results on VOC, COCO-standard, and
COCO-additional using fewer FLOPs than previous methods. To the best of our
knowledge, this is the first attempt to apply Semi-Supervised Object Detection
to YOLOv5.Comment: 14 page
Radar-STDA: A High-Performance Spatial-Temporal Denoising Autoencoder for Interference Mitigation of FMCW Radars
With its small size, low cost and all-weather operation, millimeter-wave
radar can accurately measure the distance, azimuth and radial velocity of a
target compared to other traffic sensors. However, in practice, millimeter-wave
radars are plagued by various interferences, leading to a drop in target
detection accuracy or even failure to detect targets. This is undesirable in
autonomous vehicles and traffic surveillance, as it is likely to threaten human
life and cause property damage. Therefore, interference mitigation is of great
significance for millimeter-wave radar-based target detection. Currently, the
development of deep learning is rapid, but existing deep learning-based
interference mitigation models still have great limitations in terms of model
size and inference speed. For these reasons, we propose Radar-STDA, a
Radar-Spatial Temporal Denoising Autoencoder. Radar-STDA is an efficient
nano-level denoising autoencoder that takes into account both spatial and
temporal information of range-Doppler maps. Among other methods, it achieves a
maximum SINR of 17.08 dB with only 140,000 parameters. It obtains 207.6 FPS on
an RTX A4000 GPU and 56.8 FPS on an NVIDIA Jetson AGXXavier respectively when
denoising range-Doppler maps for three consecutive frames. Moreover, we release
a synthetic data set called Ra-inf for the task, which involves 384,769
range-Doppler maps with various clutters from objects of no interest and
receiver noise in realistic scenarios. To the best of our knowledge, Ra-inf is
the first synthetic dataset of radar interference. To support the community,
our research is open-source via the link
\url{https://github.com/GuanRunwei/rd_map_temporal_spatial_denoising_autoencoder}
Unraveling the Prognostic Significance of Rgs Gene Family in Gastric Cancer and the Potential Implication of Rgs4 in Regulating Tumor-infiltrating Fibroblast
Regulator of G-protein signaling (RGS) proteins are regulators of signal transduction mediated by G protein-coupled receptors (GPCRs). Current studies have shown that some molecules in the RGS gene family are related to the occurrence, development and poor prognosis of malignant tumors. However, the RGS gene family has been rarely studied in gastric cancer. In this study, we explored the mutation and expression profile of RGS gene family in gastric cancer, and evaluated the prognostic value of RGS expression. Then we established a prognostic model based on RGS gene family and performed functional analysis. Further studies showed that RGS4, as an independent prognostic predictor, may play an important role in regulating fibroblasts in the immune microenvironment. In conclusion, this study explores the value of RGS gene family in gastric cancer, which is of great significance for predicting the prognosis and guiding the treatment of gastric cancer
Dual Immunotherapy in advanced or Metastatic Non-Small Cell Lung Cancer: a Network Meta-Analysis
OBJECTIVES: Recently, there has been extensive research on dual immunotherapy for advanced or metastatic non-small cell lung cancer (NSCLC), yet a comprehensive evaluation is lacking. This study aimed to rank the available treatment options and assess the efficacy and safety of dual immunotherapy regimens through the implementation of a Bayesian network meta-analysis (NMA).
MATERIALS AND METHODS: A thorough search was conducted to recognize eligible randomized controlled trials (RCTs) on March 20, 2023. Overall survival (OS), progression-free survival (PFS), treatment-related adverse events (TRAEs) and grade ā„3 TRAEs were evaluated to identify the efficacy and safety of dual immunotherapy regimens. The surface under the cumulative ranking curve (SUCRA) and
RESULTS: Eleven clinical trials involving six different regimens were included in this study. The combination of anti-programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) antibodies with anti-T-cell immunoglobulin and ITIM domain (TIGIT) antibodies emerged as the most promising regimen for improving OS and PFS, followed by anti-PD-1/PD-L1 + anti-cytotoxic T lymphocyte antigen 4 (CTLA-4) + chemotherapy treatment and anti-PD-1/PD-L1 + anti-CTLA-4 treatment. The forest plots demonstrated that these three regimens were all superior to chemotherapy. The above results were observed in both unselected treatment line and first-line settings. The least likely to be associated with TRAEs and grade ā„3 TRAEs were respectively anti-CTLA-4 treatment and anti-PD-1/PD-L1 + anti-TIGIT treatment, with anti-PD-1/PD-L1 + anti-CTLA-4 + chemotherapy treatment to be the worst.
CONCLUSIONS: This NMA validated the promising efficacy and safety of dual immunotherapy in advanced or metastatic NSCLC. Among them, anti-PD-1/PD-L1 + anti-TIGIT regimen emerges as a highly potential therapeutic approach. Ongoing research efforts should focus on improving treatment regimens, identifying biomarkers, and managing TRAEs to optimize the patient benefits of dual immunotherapy
B7 family protein glycosylation: Promising novel targets in tumor treatment
Cancer immunotherapy, including the inhibition of immune checkpoints, improves the tumor immune microenvironment and is an effective tool for cancer therapy. More effective and alternative inhibitory targets are critical for successful immune checkpoint blockade therapy. The interaction of the immunomodulatory ligand B7 family with corresponding receptors induces or inhibits T cell responses by sending co-stimulatory and co-inhibitory signals respectively. Blocking the glycosylation of the B7 family members PD-L1, PD-L2, B7-H3, and B7-H4 inhibited the self-stability and receptor binding of these immune checkpoint proteins, leading to immunosuppression and rapid tumor progression. Therefore, regulation of glycosylation may be the āgolden keyā to relieve tumor immunosuppression. The exploration of a more precise glycosylation regulation mechanism and glycan structure of B7 family proteins is conducive to the discovery and clinical application of antibodies and small molecule inhibitors
Metformin downregulates PD-L1 expression in esophageal squamous cell catrcinoma by inhibiting IL-6 signaling pathway
Purpose: To characterize the mechanism by which metformin inhibits PD-L1 expression in esophageal squamous cell carcinoma (ESCC) and to evaluate the effect of metformin on the antitumor immune response.
Methods: The Cancer Genome Atlas (TCGA) database was used to analyze the correlations between IL-6 and prognosis and between IL-6 and PD-L1 gene expression in esophageal cancer. Reverse transcription-quantitative polymerase chain reaction (RT-PCR), Western blotting and immunofluorescence were used to study the mechanism by which metformin affects PD-L1 expression. Additionally, T cell function was assessed in a coculture system containing ESCC cells and peripheral blood mononuclear cells (PBMCs) treated with metformin or IL-6. In an
Results: The TCGA esophageal cancer data showed that IL-6 expression was positively correlated with PD-L1 expression and that patients with high IL-6 expression had a significantly lower overall survival rate than patients with low IL-6 expression. PD-L1 expression in ESCC cell lines was significantly inhibited by metformin
Conclusions: Metformin downregulated PD-L1 expression by blocking the IL-6/JAK2/STAT3 signaling pathway in ESCC, which enhanced the antitumor immune response
Unraveling the prognostic significance of RGS gene family in gastric cancer and the potential implication of RGS4 in regulating tumor-infiltrating fibroblast
Regulator of G-protein signaling (RGS) proteins are regulators of signal transduction mediated by G protein-coupled receptors (GPCRs). Current studies have shown that some molecules in the RGS gene family are related to the occurrence, development and poor prognosis of malignant tumors. However, the RGS gene family has been rarely studied in gastric cancer. In this study, we explored the mutation and expression profile of RGS gene family in gastric cancer, and evaluated the prognostic value of RGS expression. Then we established a prognostic model based on RGS gene family and performed functional analysis. Further studies showed that RGS4, as an independent prognostic predictor, may play an important role in regulating fibroblasts in the immune microenvironment. In conclusion, this study explores the value of RGS gene family in gastric cancer, which is of great significance for predicting the prognosis and guiding the treatment of gastric cancer
The regulation and potential role of interleukin-32 in tuberculous pleural effusion
The possible protective effect of interleukin-32 (IL-32) in Mycobacterium tuberculosis (Mtb) infection has been indicated. However, few studies have been focused on IL-32 in tuberculosis patients. Additionally, the regulation of IL-32 production has rarely been reported. In the present study, the production, regulation, and role of IL-32 in tuberculous pleurisy (TBP) were investigated. We found that the content of IL-32 in tuberculous pleural effusion (TPE) was higher than the level in the malignant pleural effusion and transudative pleural effusion. The level of IL-32 mRNA in pleural fluid mononuclear cells (PFMCs) was higher than that in peripheral blood mononuclear cells (PBMCs) of patients with TBP, and this difference was mainly reflected in the splice variants of IL-32Ī±, IL-32Ī², and IL-32Ī³. Compared with the PBMCs, PFMCs featured higher IL-32Ī²/IL-32Ī³ and IL-32Ī±/IL-32Ī³ ratios. In addition, lipopolysaccharide (LPS), Bacillus Calmette-GuĆ©rin (BCG), and H37Ra stimulation could induce IL-32 production in the PFMCs. IL-32 production was positively correlated with the TNF-Ī±, IFNāĪ³, and IL-1Ra levels in TPE, whereas IFN-Ī³, but not TNF-Ī± or IL-1Ra, could induce the production of IL-32 in PFMCs. Furthermore, IL-32Ī³ could induce the TNF-Ī± production in PFMCs. Monocytes and macrophages were the main sources of IL-32 in PFMCs. Nevertheless, direct cellācell contact between lymphocytes and monocytes/macrophages plays an important role in enhancing IL-32 production by monocyte/macrophage cells. Finally, compared with the non-tuberculous pleural effusion, the purified CD4+ and CD8+ T cells in TPE expressed higher levels of intracellular IL-32. Our results suggested that, as a potential biomarker, IL-32 may play an essential role in the protection against Mtb infection in patients with TBP. However, further studies need to be carried out to clarify the functions and mechanisms of the IFN-Ī³/IL-32/TNF-Ī± axis in patients with TBP
Reactivation of mutant p53 in esophageal squamous cell carcinoma by isothiocyanate inhibits tumor growth
p53 mutations are prevalent in human cancers; approximately half of patients with esophageal cancer present these mutations. Mutant p53 (mutp53) exerts oncogenic functions that promote malignant tumor progression, invasion, metastasis, and drug resistance, resulting in poor prognosis. Some small molecules have been shown to mitigate the oncogenic function of mutp53 by restoring its wild-type activity. Although these molecules have been evaluated in clinical trials, none have been successfully used in the clinic. Here, we investigated the antitumor effects of phenethyl isothiocyanate (PEITC) in p53-mutant esophageal squamous cell carcinoma (ESCC) and elucidated its mechanism to identify new therapeutic strategies. We observed that p53R248Q is a DNA contact mutation and a structural mutation and that PEITC can restore the activity of p53R248Qin vitro and in vivo, further clarifying the antitumor activity of PEITC in cancers with different types of p53 mutations. PEITC can inhibit ESCC growth, induce apoptosis, and arrest cell cycle progression and has a preferential selectivity for ESCC with p53 mutations. Mechanistic studies showed that PEITC induced apoptosis and arrested cells at G2/M transition in cells expressing the p53R248Q mutant by restoring the wild-type conformation and transactivation function of p53; these effects were concentration dependent. Furthermore, PEITC inhibited the growth of subcutaneous xenografts in vivo and restored p53 mutant activity in xenografts. According to these findings, PEITC has antitumor effects, with its ability to restore p53R248Q activity being a key molecular event responsible for these effects
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