Hepatocellular carcinoma (referred to as liver cancer) tumor microenvironment (TMEs) is a dynamic network system composed of stromal cells, such as liver cancer cells, immune cells, vascular endothelial cells, adipocytes, fibroblasts, and various cytokines that play an important role in the invasion and metastasis of liver cancer. In recent years, there has been an increasing attention on the role of exosomes in the remodeling and the regulation of invasion and metastasis in liver cancer TMEs. Exosomes, as a natural carrier, mediate intercellular communication between liver cancer cells and with other stromal cells, playing an important role in the formation of immunosuppressive TMEs, angiogenesis and hypoxia tolerance, and the coordination of heterogeneity among liver cancer cells. This review summarizes the composition of liver cancer TMEs, the biological functions of exosomes, and the role and mechanism of exosome-mediated liver cancer TMEs between liver cancer cells and other stromal cells, with a focus on exosome involvement in the remodeling and regulating invasion and metastasis in liver cancer TMEs. Simultaneously, it also introduces and explores the application of exosomes in the diagnosis and treatment of liver cancer, with the hope that in-depth research and elucidation of the mechanisms of exosome involvement in the remodeling and regulation of invasion and metastasis in liver cancer TMEs will provide feasible research ideas for novel biological markers and drug delivery carriers.

Objective To explore the correlation between serum metabolomics characteristics and the risk of myocardial infarction in patients with coronary atherosclerosis(CAS)so as to provide new ideas and targets for clinical prevention and treatment of myocardial infarction.Methods A total of 180 CAS patients treated in our hospital from June 2018 to June 2022 were selected as the study subjects and divided into control group(non-myocardial infarction,n=138)and observation group(myocardial infarction,n=42)according to follow-up.Propensity score matching method was used to perform 1∶1 matching,and a total of 34 pairs were successfully matched.The serum samples of patients were detected by mass spectrometry chip in metabolomics technology.Principal component analysis(PCA),partial least square discriminant analysis(PLS-DA),and orthogonal partial least square discriminant analysis(OPLS-DA)results were compared among groups to screen out different metabolites.The diagnostic value of differential metabolites was evaluated by receiver operating characteristic(ROC)curve.The samples were cluster analyzed by agglomerative hierarchical clustering,and the pathway enrichment analysis of differential metabolites was carried out.Results There were significant differences in the mass spectra of serum samples from the two groups of CAS patients.PC A results showed that there was a certain separation trend between the overall level of serum metabolism in the two groups,but the trend was not significant(R2X=0.654,Q2Y=0.719).PLS-DA analysis showed the separation trend of the two groups of samples(R2X=0.582,R2Y=0.810,Q2Y=0.675).Further OPLS-DA analysis showed that the two groups of samples had an obvious separation trend(R2X=0.595,R2Y=0.831,Q2Y=0.742).Twelve differential metabolites between groups were screened by VIP value＞1 and Wilcoon-Mann-Whitney test;of them three were upregulated and nine were downregulated.Upregulated D-glucose and downregulated glycocholic acid,ursodeoxycholic acid,nicotinic acid acid,niacinamide and succinic acid were of high value as diagnostic markers for myocardial infarction.Differential metabolite pathway analysis showed that among the eight metabolic pathways that may be disturbed by differential metabolites,non-alcoholic fatty liver,niacin and niacinamide metabolism,and pathways associated with type 2 diabetes mellitus Impact ≥ 0.1 might be potential pathways in the pathogenesis of myocardial infarction in CAS patients.Conclusion Serum levels of glycinocholic acid,D-glucose,ursodeoxycholic acid,niacin,niacinamide,and succinic acid can be used as potential markers to distinguish the risk of myocardial infarction in patients with CAS.The metabolic pathways affected mainly include non-alcoholic fatty liver disease,niacin and niacinamide metabolism,and type 2 diabetes mellitus-related pathways.

Objective To explore the correlation between serum metabolomics characteristics and the risk of myocardial infarction in patients with coronary atherosclerosis(CAS)so as to provide new ideas and targets for clinical prevention and treatment of myocardial infarction.Methods A total of 180 CAS patients treated in our hospital from June 2018 to June 2022 were selected as the study subjects and divided into control group(non-myocardial infarction,n=138)and observation group(myocardial infarction,n=42)according to follow-up.Propensity score matching method was used to perform 1∶1 matching,and a total of 34 pairs were successfully matched.The serum samples of patients were detected by mass spectrometry chip in metabolomics technology.Principal component analysis(PCA),partial least square discriminant analysis(PLS-DA),and orthogonal partial least square discriminant analysis(OPLS-DA)results were compared among groups to screen out different metabolites.The diagnostic value of differential metabolites was evaluated by receiver operating characteristic(ROC)curve.The samples were cluster analyzed by agglomerative hierarchical clustering,and the pathway enrichment analysis of differential metabolites was carried out.Results There were significant differences in the mass spectra of serum samples from the two groups of CAS patients.PC A results showed that there was a certain separation trend between the overall level of serum metabolism in the two groups,but the trend was not significant(R2X=0.654,Q2Y=0.719).PLS-DA analysis showed the separation trend of the two groups of samples(R2X=0.582,R2Y=0.810,Q2Y=0.675).Further OPLS-DA analysis showed that the two groups of samples had an obvious separation trend(R2X=0.595,R2Y=0.831,Q2Y=0.742).Twelve differential metabolites between groups were screened by VIP value＞1 and Wilcoon-Mann-Whitney test;of them three were upregulated and nine were downregulated.Upregulated D-glucose and downregulated glycocholic acid,ursodeoxycholic acid,nicotinic acid acid,niacinamide and succinic acid were of high value as diagnostic markers for myocardial infarction.Differential metabolite pathway analysis showed that among the eight metabolic pathways that may be disturbed by differential metabolites,non-alcoholic fatty liver,niacin and niacinamide metabolism,and pathways associated with type 2 diabetes mellitus Impact ≥ 0.1 might be potential pathways in the pathogenesis of myocardial infarction in CAS patients.Conclusion Serum levels of glycinocholic acid,D-glucose,ursodeoxycholic acid,niacin,niacinamide,and succinic acid can be used as potential markers to distinguish the risk of myocardial infarction in patients with CAS.The metabolic pathways affected mainly include non-alcoholic fatty liver disease,niacin and niacinamide metabolism,and type 2 diabetes mellitus-related pathways.

Hepatocellular carcinoma (referred to as liver cancer) tumor microenvironment (TMEs) is a dynamic network system composed of stromal cells, such as liver cancer cells, immune cells, vascular endothelial cells, adipocytes, fibroblasts, and various cytokines that play an important role in the invasion and metastasis of liver cancer. In recent years, there has been an increasing attention on the role of exosomes in the remodeling and the regulation of invasion and metastasis in liver cancer TMEs. Exosomes, as a natural carrier, mediate intercellular communication between liver cancer cells and with other stromal cells, playing an important role in the formation of immunosuppressive TMEs, angiogenesis and hypoxia tolerance, and the coordination of heterogeneity among liver cancer cells. This review summarizes the composition of liver cancer TMEs, the biological functions of exosomes, and the role and mechanism of exosome-mediated liver cancer TMEs between liver cancer cells and other stromal cells, with a focus on exosome involvement in the remodeling and regulating invasion and metastasis in liver cancer TMEs. Simultaneously, it also introduces and explores the application of exosomes in the diagnosis and treatment of liver cancer, with the hope that in-depth research and elucidation of the mechanisms of exosome involvement in the remodeling and regulation of invasion and metastasis in liver cancer TMEs will provide feasible research ideas for novel biological markers and drug delivery carriers.

Hepatic sinusoidal obstruction syndrome (HSOS) is a type of secondary vascular disease of the liver that is mainly associated with the ingestion of pyrrole alkaloids (PAs) and hematopoietic stem cell transplantation (HSCT) treatment, resulting in severe liver dysfunction, multiple organ failure, and even death. Hepatic sinusoidal dilatation and obstruction, hepatocyte coagulative necrosis, and hepatic lobular inflammation are the main pathological manifestations of HSOS. The key initiating process for the pathogenesis of HSOS is damage to liver sinusoidal endothelial cells (LSECs). Currently, it is believed that LSECs are damaged by the involvement of multiple etiologies and mechanisms, and secondary coagulation and fibrinolysis disorders, oxidative stress, and inflammatory responses are the occurrence contributors to HSOS; however, the mechanism has not been fully elucidated. Therefore, the role of immune-inflammatory mechanisms has received increasing attention in LSEC damage. This article provides an overview of the epidemiology, etiology, and pathological changes of HSOS and reviews the physiological functions, common etiological damage mechanisms, and the key role of LSEC damage in the pathogenesis of HSOS, with a special focus on the role and research progress of immune-inflammatory mechanisms for LSEC damage in recent years. Furthermore, we believe that in-depth study and elucidation of the role of immune-inflammatory mechanisms in LSEC damage and the pathogenesis of HSOS and diagnosis will provide feasible research and development ideas for the screening and identification of new markers and drug treatment targets for HSOS.

The incidence and mortality rates of cholangiocarcinoma (CCA) are increasing constantly, and it is of great importance to explore new therapeutic targets. Ferroptosis, a unique pattern of cell death caused by iron-dependent cellular oxidative injury, is closely associated with iron metabolism and oxidative stress imbalance in cancer and has become a research hotspot in the field of tumor. This article introduces the mechanism of ferroptosis and the research advances in ferroptosis involved in the development and progression of CCA, and it is pointed out that the regulatory mechanism of ferroptosis has an important clinical value in the malignant progression of CCA.

In recent years, with the changes in living standards and dietary structure, the incidence of non-alcoholic fatty liver disease has been increasing year by year in China, and the incidence rate in the general population is as high as 29.81%. An increasingly epidemiological evidence suggests that non-alcoholic fatty liver disease has become one of the causes of increasing liver cirrhosis and liver cancer. However, its etiology and pathogenesis are complex and have not yet been fully elucidated. Therefore, establishing an appropriate non-alcoholic fatty liver disease animal models for pre-clinical research is essential to elucidate its pathogenesis. This article summarizes the latest research progress of non-alcoholic fatty liver disease animal models, which are common at home and abroad in recent years.

Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease in children and adults, and is closely related to obesity and metabolic factors. In recent years, with the changes in living standards and dietary structure, the incidence of NAFLD has been increasing year by year. Pediatric NAFLD has many similarities with adult NAFLD in terms of epidemiology, etiology, pathogenesis, and diagnosis and treatment strategies; however it has its own unique characteristics. This paper reviews the latest research progress of pediatric NAFLD in recent years at home and abroad.

ObjectiveTo investigate clinical features and outcomes in acute ischemic stroke patients with remote symptomatic intracranial hemorrhage (sICHr) after intravenous thrombolysis.MethodsThe acute ischemic stroke patients with sICHr after intravenous thrombolysis therapy were enrolled retrospectively.The clinical data were collected and the related literature was analyzed and summarized.ResultsA total of 6 acute ischemic stroke patients with sICHr were enrolled, including 4 males.Three patients had a history of using antiplatelet agents, 2 with atrial fibrillation, 4 with hypertension, 3 with previous stroke history, 4 with smoking history, and 4 had sICHr at 2 h after intravenous thrombolysis.Of the 14 hemorrhagic foci (except in the infarct areas), 10 were in the cerebral cortex.Three patients died within 1 week, and 1 was in a persistent vegetative state.Conclusions SICHr after intravenous thrombolysis in patients with acute ischemic stroke is mainly located in the cerebral cortex.The outcomes in acute ischemic stroke patients with SICHr after intravenous thrombolysis are poor, and the mortality is high.