Objective To summarize the papers about the research status and prospects of ferroptosis in hepatocellular carcinoma (HCC) and its drug resistance in recent years in order to provide directions and ideas for the treatment of HCC. Method The relevant literatures at home and abroad in recent years about ferroptosis in HCC and its drug resistance were reviewed. Results The mechanism of ferroptosis in the development and drug resistance of HCC was complicated, involving multiple protein and molecular pathways. Ferroptosis played an important role in improving chemotherapy and sorafenib resistance, and it had a broad application prospect in HCC. Conclusions The molecular mechanism of ferroptosis in HCC and its drug resistance has not been fully elucidated. Further research on the mechanism of ferroptosis in HCC may provide new molecular therapeutic targets for HCC. Ferroptosis has a broad application prospect in the treatment of HCC.
ObjectiveThis study aims to summarize the application and research progress of antibody-drug conjugates (ADC) in gastric cancer (GC). MethodWe reviewed recent domestic and international research on ADC in GC and conducted a comprehensive summary. ResultsADC was emerging as one of the most effective therapeutic options for advanced GC patients, significantly impacting the treatment and prognosis of these patients. However, their clinical application had certain limitations in some aspects. There were some kinds of ADC targeting human epidermal growth factor receptor-2, human epidermal growth factor receptor-3, guanylyl cyclase C, and trophoblasti surface antigen 2. Furthermore, the development of ADC with multiple mechanisms of action held great promise. ConclusionADC drugs represent a valuable approach for the treatment of GC and offer new perspectives and insights into the management of GC patients.
Fatigue driving is one of the leading causes of traffic accidents, posing a significant threat to drivers and road safety. Most existing methods focus on studying whole-brain multi-channel electroencephalogram (EEG) signals, which involve a large number of channels, complex data processing, and cumbersome wearable devices. To address this issue, this paper proposes a fatigue detection method based on frontal EEG signals and constructs a fatigue driving detection model using an asymptotic hierarchical fusion network. The model employed a hierarchical fusion strategy, integrating an attention mechanism module into the multi-level convolutional module. By utilizing both cross-attention and self-attention mechanisms, it effectively fused the hierarchical semantic features of power spectral density (PSD) and differential entropy (DE), enhancing the learning of feature dependencies and interactions. Experimental validation was conducted on the public SEED-VIG dataset. The proposed model achieved an accuracy of 89.80% using only four frontal EEG channels. Comparative experiments with existing methods demonstrate that the proposed model achieves high accuracy and superior practicality, providing valuable technical support for fatigue driving monitoring and prevention.
Diabetic retinopathy (DR) is a serious complication of diabetes mellitus that not only impairs vision and quality of life but has also emerged as a leading cause of blindness in working-age individuals. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (LncMALAT1) is a non-coding RNA molecule that regulates gene expression and has been implicated in the pathogenesis and progression of DR. It exerts its effects through the modulation of various pathological processes, including inflammation, oxidative stress, angiogenesis, and apoptosis. Notably, alterations in the expression levels of LncMALAT1 may serve as potential biomarkers for the early diagnosis of DR. Furthermore, interventions targeting LncMALAT1, employing antioxidants, anti-angiogenic agents, traditional Chinese medicine, and gene therapy, present promising avenues for its potential development as an effective therapeutic target for DR.
Objective To explore the potential roles and mechanism of Wnt5a and its receptors in the pathogenesis of bronchiectasis. Methods From October 2017 to April 2018, outpatients with bronchiectasis who needed bronchoscopy were recruited in the Department of Respiratory and Critical Care Medicine of West China Hospital of Sichuan University. The control group was patients with pulmonary nodules less than 10 mm in diameter by health inspection. Patients who used antibiotics and/or glucocorticoids within the past 4 weeks or had other airway diseases were excluded. Serum and bronchial mucosa were collected for detection of Wnt5a by enzyme-linked immunosorbent assay and real-time polymerase chain reaction (PCR), respectively. The receptor of Wnt5a, Ror2, and the downstream pro-inflammatory cytokines, interleukin (IL)-1β and IL-6, were measured in the bronchial mucosa by real-time PCR. Results From October 2017 to April 2018, 32 outpatients with bronchiectasis were found but only 17 patients finished this study, and simultaneously 18 patients with pulmonary nodules were chosen as control. The level of serum Wnt5a in patients with bronchiectasis were significantly higher than that in the control group (P<0.05). Correlation analyses showed that serum Wnt5a level was positively correlated with the level of serum C reactive protein (r=0.806, P<0.05), but had no relation with the level of white blood cell count, blood neutrophil percentage, pulmonary function or bronchiectasis severe index. The mRNA levels of Wnt5a and its receptor Ror2 in bronchial mucosa of patients with bronchiectasis were significantly higher than those in the control group (P<0.001). The mRNA levels of IL-1β and IL-6 in bronchial mucosa of patients with bronchiectasis were higher than those in the control group (P<0.05). Conclusion Wnt5a may play crucial roles in the development of bronchiectasis through Wnt5a/Ror2 signaling pathways to regulate the release of pro-inflammatory cytokines including IL-1β and IL-6.
ObjectiveTo understand the molecular mechanisms and targeted therapy research progress of gastric cancer associated with the RTK/RAS signaling pathway, in order to provide reference for treatment of gastric cancer. MethodThe related literatures about the molecular mechanism and targeted therapy of RTK/RAS signaling pathway related gastric cancer at home and abroad in recent years were reviewed. ResultsTargeted therapy had been widely applied in the treatment of gastric cancer associated with the RTK/RAS signaling pathway, showing good efficacy and significantly prolonging patients’ survival time, further deepening the understanding of the molecular mechanisms of gastric cancer. Targeted therapies for gastric cancer associated with the RTK/RAS signaling pathway focused on human epidermal growth factor receptor 2 (HER-2), epidermal growth factor receptor, fibroblast growth factor receptor 2, cellular-mesenchymalepithelial transition factor and Kirsten ratsarcoma viral oncogene homolog associated targets. Currently, there were many drugs targeting HER-2 target, while research on other targets mostly remains in the clinical trial stage, and showing promising prospects. ConclusionTargeted therapy can benefit most patients with gastric cancer, but the drug resistance and multi-drug combination therapy are still difficult problems that we need to overcome in the future.
Iron death is an alternative to normal cell death and is regulated by a variety of cellular metabolic pathways. Iron death has become a hot topic of research because it can cause damage to various organs and degenerative diseases in the body. Metabolism, signalling pathways, endoplasmic reticulum stress, and immune cells can all affect the occurrence of iron death, and the blood-retina destruction induced by iron death plays an important role in autoimmune uveitis. Exploring the components of the blood-retina regulatory mechanism of iron death in autoimmune uveitis can lead to the search for targeted drug targets, which can provide a new research idea for the subsequent study of the diagnosis and treatment of autoimmune uveitis.
Objective To investigate the effects of repeated shortischemia training on flap survival area, vascular endothelial growth factor and the microvascularsel density. Methods Seventy-two rabbits were divided into:the experimental group(n=64), the skin flaps were constructed in two sides of back, one side flap were given ischemia training for 15 minutes and 8 times one day at the pedicles from the 1st to 8th day after operation (group A), the other side flap was served as a control (group B), the corresponding site was only marked as a blank control group (group C).Then, 8 pedicles of group A and group Bwere isolated every day. The surviving area of all skin flaps were calculated on the5th day after isolating operation. The vascular endothelial growth factor(VEGF)and microvessel density(MVD) of the 3 groups were checked with immunohistologochemical staining. Results After the operation, all animalswere survival with normal vitality.The survival flap area of group A were significant more than that of group B after 3 days(Plt;0.05).The expressions of VEGF and MVD of group A and group B were higher than group C. The expression of VEGF of group A was significantly higher than that of group B(Plt;0.01). The counting of MVD of group A was also significantly higher than that of group B(Plt;0.05). There was positive correlation between flap survival area and MVD in group A. The relation of time point was n and n 2 respectively,correlation coefficient was 0.850. As well as MVD and VEGF were positive correlation,correlation coefficient was 0.801. Conclusion Early repeated shortischemia training can increase flap survival area, the mechanism maybe involve the increased expression of VEGF, which can increased skin flap microvascular density.
Objective To investigate the pharmacological effects and mechanisms of natural medicine artemisinin and its derivatives. Methods The pertinent domestic and overseas literatures of recent years were reviewed and summarized. Results Artemisinin and its derivatives have unique structure, high efficiency with low toxicity. The pharmacological effects include anti-malaria, anti-tumor, immune function regulation, anti-bacterial, anti-fetation, anti-fibrosis, heat-clearing and detoxicating, etc. Conclusion Artemisinin and its derivatives play pharmacological effects in different ways, and have a good foreground in the application.
ObjectiveAlthough evidence links idiopathic pulmonary fibrosis (IPF) and diabetes mellitus (DM), the exact underlying common mechanism of its occurrence is unclear. This study aims to explore further the molecular mechanism between these two diseases. MethodsThe microarray data of idiopathic pulmonary fibrosis and diabetes mellitus in the Gene Expression Omnibus (GEO) database were downloaded. Weighted Gene Co-Expression Network Analysis (WGCNA) was used to identify co-expression genes related to idiopathic pulmonary fibrosis and diabetes mellitus. Subsequently, differentially expressed genes (DEGs) analysis and three public databases were employed to analyze and screen the gene targets related to idiopathic pulmonary fibrosis and diabetes mellitus. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Metascape. In addition, common microRNAs (miRNAs), common in idiopathic pulmonary fibrosis and diabetes mellitus, were obtained from the Human microRNA Disease Database (HMDD), and their target genes were predicted by miRTarbase. Finally, we constructed a common miRNAs-mRNAs network by using the overlapping genes of the target gene and the shared gene. ResultsThe results of common gene analysis suggested that remodeling of the extracellular matrix might be a key factor in the interconnection of DM and IPF. Finally, hub genes (MMP1, IL1R1, SPP1) were further screened. miRNA-gene network suggested that has-let-19a-3p may play a key role in the common molecular mechanism between IPF and DM. ConclusionsThis study provides new insights into the potential pathogenic mechanisms between idiopathic pulmonary fibrosis and diabetes mellitus. These common pathways and hub genes may provide new ideas for further experimental studies.