ABSTRACT
Breast cancer has a high incidence and a heightened propensity for metastasis. The absence of precise targets for effective intervention makes it imperative to devise enhanced treatment strategies. Exosomes, characterized by a lipid bilayer and ranging in size from 30 to 150 nm, can be actively released by various cells, including those in tumors. Exosomes derived from distinct subsets of immune cells have been shown to modulate the immune microenvironment within tumors and influence breast cancer progression. In addition, tumor-derived exosomes have been shown to contribute to breast cancer development and progression and may become a new target for breast cancer immunotherapy. Tumor immunotherapy has become an option for managing tumors, and exosomes have become therapeutic vectors that can be used for various pathological conditions. Edited exosomes can be used as nanoscale drug delivery systems for breast cancer therapy, contributing to the remodeling of immunosuppressive tumor microenvironments and influencing the efficacy of immunotherapy. This review discusses the regulatory role of exosomes from different cells in breast cancer and the latest applications of exosomes as nanoscale drug delivery systems and immunotherapeutic agents in breast cancer, showing the development prospects of exosomes in the clinical treatment of breast cancer.
Subject(s)
Breast Neoplasms , Exosomes , Immunotherapy , Tumor Microenvironment , Exosomes/immunology , Exosomes/metabolism , Humans , Breast Neoplasms/therapy , Breast Neoplasms/immunology , Female , Immunotherapy/methods , Tumor Microenvironment/immunology , Animals , Drug Delivery SystemsABSTRACT
Surface defect detection of strip steel is an important guarantee for improving the production quality of strip steel. However, due to the diverse types, scales, and texture structures of surface defects on strip steel, as well as the irregular distribution of defects, it is difficult to achieve rapid and accurate detection of strip steel surface defects with existing methods. This article proposes a real-time and high-precision surface defect detection algorithm for strip steel based on YOLOv7. Firstly, Partial Conv is used to replace the conventional convolution blocks of the backbone network to reduce the size of the network model and improve the speed of detection; Secondly, The CA attention mechanism module is added to the ELAN module to enhance the ability of the network to extract detect features and improve the effectiveness of detect detection in complex environments; Finally, The SPD convolution module is introduced at the output end to improve the detection performance of small targets with surface defects on steel. The experimental results on the NEU-DET dataset indicate that the mean average accuracy (mAP@IoU = 0.5) is 80.4%, which is 4.0% higher than the baseline network. The number of parameters is reduced by 8.9%, and the computational load is reduced by 21.9% (GFLOPs). The detection speed reaches 90.9 FPS, which can well meet the requirements of real-time detection.
ABSTRACT
BACKGROUND: Combined pituitary hormone deficiency 3 (CPHD3; OMIM: 221750) is caused by mutations within the LHX3 gene (OMIM: 600577), which located on the subtelomeric region of chromosome 9 at band 9q34.3, has seven coding exons and six introns. LIM homeobox (LHX) 3 protein is the key regulator of pituitary development in fetal life. CASE SUMMARY: We have diagnosed and treate an 11-year-old boy with combined pituitary hormone deficiency (CPHD). The main clinical manifestations were pituitary hormone deficiency, hydrocele of the tunica vaginalis, pituitary dwarfism, gonadal dysplasia, micropenis, clonic convulsion, and mild facial dysmorphic features. We collected peripheral blood from the patient, the patient's older brother, as well as their parents, and sequenced them by using high-throughput whole-exosome sequencing, which was verified by Sanger sequencing. The results showed that there were two compound heterozygous variants of c.613G>C (p.V205L) and c.220T>C (p.C74R) in the LHX3 gene. c.613G>C (p.V205L) was inherited from his mother and c.220T>C (p.C74R) from his father. His brother also has both variants and symptoms. CONCLUSION: This study reported ununreported genetic mutations of LHX3, and recorded the treatment process of the patients, providing data for the diagnosis and treatment of CPHD.
