China is one of the countries in the world with the highest rate of esophageal cancer. Early detection, accurate diagnosis, and treatment of esophageal cancer are critical for improving patients’ prognosis and survival. Machine learning technology has become widely used in cancer, which is benefited from the accumulation of medical images and advancement of artificial intelligence technology. Therefore, the learning model, image type, data type and application efficiency of current machine learning technology in esophageal cancer are summarized in this review. The major challenges are identified, and solutions are proposed in medical image machine learning for esophageal cancer. Machine learning's potential future directions in esophageal cancer diagnosis and treatment are discussed, with a focus on the possibility of establishing a link between medical images and molecular mechanisms. The general rules of machine learning application in the medical field are summarized and forecasted on this foundation. By drawing on the advanced achievements of machine learning in other cancers and focusing on interdisciplinary cooperation, esophageal cancer research will be effectively promoted.
Psilocybin is a hallucinogenic indole alkaloid derived from mushrooms, which is metabolized into psilocin in vivo and exerts biological effects. Clinical studies have shown that psilocybin has the effect of relieving anxiety and depression in cancer patients. Due to its fast onset, significant therapeutic effect, and low addictive nature, psilocybin has the potential to break through the bottleneck of slow action and poor efficacy of existing depression drugs, bringing new hope for the treatment of severe depression and refractory depression. This article will review the pharmacokinetics, antidepressant mechanisms, and research progress of psilocybin, providing a reference for subsequent research.
[Abstract]Bone metastasis is one of the common complications of lung cancer, which seriously affects the quality of life and survival of patients. At present, the clinical diagnosis of bone metastasis of lung cancer mainly depends on imaging methods, but due to its lack of sensitivity and potential radiation risk, about half of patients have already had bone-related events when they are diagnosed clearly. The treatment of bone metastasis of lung cancer mainly depends on surgery, radiotherapy and chemotherapy, targeted therapy, immunosuppressants, etc. Although the treatment of bone metastasis of lung cancer has made some progress in recent years, there are still some problems such as high risk of other distant metastasis. This article mainly reviews the pathogenesis, diagnostic biomarkers and treatment progress of bone metastasis of lung cancer, in order to provide reference for the diagnosis and treatment of bone metastasis of lung cancer.
ObjectiveTo summarize the relationship between exosomes and the occurrence and development of gastrointestinal cancer.MethodsThrough online database, we collected the literatures about the relationship between exosomes and the development of gastrointestinal cancer at home and abroad, and then made an review.ResultsExosomes secreted by gastrointestinal cancer cells were related to tumorigenesis, tumor cell survival, chemoresistance, and early metastasis. Exosomes could play the role of information transmission, and regulation of cell physiology and pathological process in the development of gastrointestinal cancer through a variety of intercellular binding ways, and affectted the occurrence and development of gastrointestinal cancer via epigenetic regulation and tumor related signal transduction mechanism. They had been proved to be biomarkers, targets, and drug carriers for the treatment of gastrointestinalcancer.ConclusionIt is a new way to explore the molecular mechanism of exosomes in the development of gastrointestinal cancer.
Obesity is a prevalent metabolic disorder,which seriously affects human health and has become the world's public health problem. Kinase S6K1, an important downstream effector of mammalian target of rapamycin (mTOR), influences specific pathological responses, including obesity, type 2 diabetes and cancer. Presently, S6K1 has become an attractive therapeutic target in the treatment of these disorders. Here, the functions of kinase S6K1, its molecular regulation mechanisms, related pathogenesis of disease and relevant small molecular inhibitors are reviewed. Finally, the prospect of research toward S6K1 is expected as well.
ObjectiveTo explore the differentially expressed genes (DEGs) in venous leg ulcer (VLU) by bioinformatics, and further explore the molecular mechanism of the disease, predict early diagnostic markers and treatment targets.MethodsThe expression profiles of VLU were downloaded from the gene expression omnibus (GEO) database, the DEGs of VLU and inflammatory phase of normal skin healing were identified by R software and used to perform gene ontology (GO) and KEGG pathway enrichment analysis, obtaining the key genes of the pathway. We analyzed the proteins of protein interaction (PPI) network by STRING database and Cytoscape 3.2.1 software to obtain hub genes.ResultsA total of 409 DEGs were obtained, including 173 upregulted genes and 236 downregulted genes. The GO analysis showed that the upregulated DEGs mainly distributed in collagen-containing extracellular matrix (ECM), cornified envelope and collagen trimer, involved in biological processes such as skin development, keratinocyte differentiation and cornification, which mediated molecular functions such as ECM structural constituent, ECM structural constituent conferring tensile strength and integrin binding. The downregulated DEGs mainly distributed in tertiary granule, secretory granule membrane and tertiary granule membrane cornification, involved in biological processes such as response to chemokine, leukocyte migration and neutrophil chemotaxis, which mediated molecular functions such as chemokine activity, chemokine receptor binding and cytokine activity. KEGG pathway enrichment analysis results showed that the upregulated DEGs were mainly enriched in ECM-receptor interaction and protein digestion and absorption pathways, collagen type Ⅰ alpha1 chain (COL1A1), collagen type Ⅰ alpha2 chain (COL1A2), and collagen type Ⅵ alpha 6 chain (COL6A6) were the key genes of pathway; the downregulated DEGs were mainly enriched in Staphylococcus aureus infection, Toll-like receptor signaling pathway and leukocyte transendothelial migration pathways, interleukin (IL)-1β, C-X-C motif chemokine ligand 8 (CXCL8), IL-10, matrix metalloproteinase (MMP)1, and MMP9 were the key genes of pathway. The hub core genes of the PPI network were formyl peptide receptor (FPR)1, FPR2, IL-1β, IL-10, and CXCL8.ConclusionsThe results of this study indicate that the genes and signaling pathways involved in COL1A1, COL1A2, COL6A6, IL-1β, CXCL8, IL-10, MMP1, and MMP9 affect the healing of VLU. FPR1, FPR2, IL-1β, IL-10, and CXCL8 can be used as potential therapeutic targets.
Endogenous adult neural stem cells are closely related to the normal physiological functions of the brain and many neurodegenerative diseases. Neurons are affected by factors such as extracellular microenvironment and intracellular signaling. In recent years, some specific signaling pathways have been found that affect the occurrence of neural stem cells in adult neural networks, including proliferation, differentiation, maturation, migration, and integration with host functions. In this paper, we summarize the signals and their molecular mechanisms, including the related signaling pathways, neurotrophic factors, neurotransmitters, intracellular transcription factors and epigenetic regulation of neuronal differentiation from both the extracellular and intracellular aspects, providing basic theoretical support for the treatment of central nervous system diseases through neural stem cells approach.
Intervertebral disc degeneration is a multifactorial pathological process which is one of the leading causes of disability worldwide. The main pathological changes of intervertebral disc degeneration are the degradation of extracellular matrix, apoptosis, autophagy, senescence and inflammation. Dysregulation of microRNAs has been implicated in various pathologies, including various degenerative diseases such as disc degeneration. This article reviews the research status of microRNA in degenerative disc pathology, with emphasis on the biological mechanisms and potential therapeutic prospects of microRNA in extracellular matrix degradation, apoptosis, inflammation, and cartilage endplate degeneration.
At present, the potential hazards of infrasound on heart health have been identified in previous studies, but a comprehensive review of its mechanisms is still lacking. Therefore, this paper reviews the direct and indirect effects of infrasound on cardiac function and explores the mechanisms by which it may induce cardiac abnormalities. Additionally, in order to further study infrasound waves and take effective preventive measures, this paper reviews the mechanisms of cardiac cell damage caused by infrasound exposure, including alterations in cell membrane structure, modulation of electrophysiological properties, and the biological effects triggered by neuroendocrine pathways, and assesses the impact of infrasound exposure on public health.
PNAS-4 is a novel pro-apoptosis gene identified latetly. In recent years, there has been a large number of research reports on the basic studies about PNAS-4 in cancer gene therapy and gene therapy of PNAS-4 alone or combined with chemotherapy or radiotherapy manifested a good application prospect, but its molecular mechanisms to promote apoptosis is not clear yet. In this paper, recent research about PNAS-4 in cancer gene therapy is briefly reviewed, and recent hypotheses on its molecular mechanisms to promote apoptosis are especially elucidated. Based on its newly identified characteristics of structural domain, we made a point that PNAS-4 might regulate functions of some target protein related to apoptosis by deSumoylation as a new deSumoylating isopeptidase, and consequently promote apoptosis.