Crosstalk between endothelial progenitor cells and HCC through periostin/CCL2/CD36 supports formation of the pro-metastatic microenvironment in HCC.

Metastasis causes most cancer-related deaths, and the role and mechanism of periostin (POSTN) in the metastasis of hepatocellular carcinoma (HCC) remain undiscovered. In this study, DEN and HTVi HCC models were performed in hepatic-specific Postn ablation and Postn knock-in mouse to reveal the role of POSTN in HCC metastasis. Furthermore, POSTN was positively correlated with circulating EPCs level and promoted EPC mobilization and tumour infiltration.

PPARβ/δ-ANGPTL4 axis mediates the promotion of mono-2-ethylhexyl phthalic acid on MYCN-amplified neuroblastoma development.

Di-2-ethylhexyl phthalic acid (DEHP) is one of the most widely used plasticizers in the industry, which can improve the flexibility and durability of plastics. It is prone to migrate from various daily plastic products through wear and leaching into the surrounding environment and decompose into the more toxic metabolite mono-2-ethylhexyl phthalic acid (MEHP) after entering the human body. However, the impacts and mechanisms of MEHP on neuroblastoma are unclear.

CDKN2B-AS1 mediates proliferation and migration of vascular smooth muscle cells induced by insulin.

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the intimal hyperplasia in type 2 diabetes mellitus (T2DM) patients after percutaneous coronary intervention. We aimed to investigate the role of lncRNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in VSMC proliferation and migration, as well as the underlying mechanism. T2DM model mice with carotid balloon injury were used in vivo and mouse aortic vascular smooth muscle cells (MOVAS) stimulated by insulin were used in vitro to assess the role of CDKN2B-AS1 in VSMC proliferation and migration following vascular injury in T2DM state.

AZGP1 activation by lenvatinib suppresses intrahepatic cholangiocarcinoma epithelial-mesenchymal transition through the TGF-β1/Smad3 pathway.

Intrahepatic cholangiocarcinoma (ICC) is a primary liver malignancy and is characterized by highly aggressive and malignant biological behavior. Currently, effective treatment strategies are limited. The effect of lenvatinib on ICC is unknown.

Associations between gut microbiota and sleep: a two-sample, bidirectional Mendelian randomization study.

Introduction: Previous research has reported that the gut microbiota performs an essential role in sleep through the microbiome-gut-brain axis. However, the causal association between gut microbiota and sleep remains undetermined.

Methods: We performed a two-sample, bidirectional Mendelian randomization (MR) analysis using genome-wide association study summary data of gut microbiota and self-reported sleep traits from the MiBioGen consortium and UK Biobank to investigate causal relationships between 119 bacterial genera and seven sleep-associated traits.

Loss of LncRNA DUXAP8 synergistically enhanced sorafenib induced ferroptosis in hepatocellular carcinoma via SLC7A11 de-palmitoylation.

Background: Ferroptosis is an important iron-dependent form of cell death in hepatocellular carcinoma (HCC). Sorafenib, a potent ferroptosis inducer, is used to treat advanced HCC but its efficacy is limited by the development of drug resistance.

Methods: The effects of DUXAP8 expression on HCC progression were evaluated by TCGA database, Kaplan-Meier analysis, and in situ hybridization analysis.

Analysis and comparison of failure causes of minimally invasive surgical closure of ventricular septal defects in children.

Objectives: The aims of the present study were to explore the causes of minimally invasive surgical ventricular septal defect (VSD) closure failure under transesophageal echocardiography guidance and thus to improve the success rate of surgical VSD closure.

Methods: From January 2015 to December 2019, 522 children with VSD underwent minimally invasive surgical closure. Nineteen procedures (3.

CAFs-derived SCUBE1 promotes malignancy and stemness through the Shh/Gli1 pathway in hepatocellular carcinoma.

Background: The tumour microenvironment and cirrhotic liver are excellent sources of cancer-associated fibroblasts (CAFs), which participate in carcinogenesis. Thus, it is important to clarify the crosstalk between CAFs and HCC cells and the related mechanism in regulating carcinogenesis.

Methods: Human hepatocellular carcinoma (HCC) tissues and matched adjacent normal tissues were obtained from HCC patients.

Gut dysfunction may be the source of pathological aggregation of alpha-synuclein in the central nervous system through Paraquat exposure in mice.

Background: One of the most common types of neurodegenerative diseases (NDDs) is Lewy body disease (LBD), which is characterized by excessive accumulation of α-synuclein (α-syn) in the neurons and affects around 6 million individuals globally. In recent years, due to the environmental factors that can affect the development of this condition, such as exposure to herbicides and pesticides, so it has become a younger disease. Currently, the vast majority of studies on the neurotoxic effects of paraquat (PQ) focus on the late mechanisms of neuronal-glial network regulation, and little is known about the early origins of this environmental factor leading to LBD.

LncRNA HEPFAL accelerates ferroptosis in hepatocellular carcinoma by regulating SLC7A11 ubiquitination.

Ferroptosis is a new type of cell death that has been recognized in recent years and is different from apoptosis, autophagy, and necrosis. It is mainly due to cellular iron homeostasis and lipid peroxidation of iron metabolism caused by large accumulation. There is a close correlation between ferroptosis and hepatocellular carcinoma (HCC).

Role of ferroptosis in gastrointestinal tumors: From mechanisms to therapies.

Ferroptosis is an iron-dependent nonapoptotic regulated cell death, which is mainly caused by an abnormal increase in lipid oxygen free radicals and an imbalance in redox homeostasis. Recently, ferroptosis has been shown to have implications in various gastrointestinal cancers, such as gastric carcinoma, hepatocellular carcinoma, and pancreatic cancer. This review summarises the latest research on ferroptosis, its mechanism of action, and its role in the progression of different gastrointestinal tumors to provide more information regarding the prevention and treatment of these tumors.

Paraquat Inhibits Autophagy Via Intensifying the Interaction Between HMGB1 and α-Synuclein.

Paraquat, a widely used herbicide, is associated with an increased risk of Parkinson's disease (PD). PQ induces upregulation and accumulation of α-synuclein in neurons, which is one of the major pathological hallmarks of PD. Autophagy, as the major mechanism for the clearance of α-synuclein, is disrupted upon pesticide exposure as well as in PD patients.

Complement C1q binding protein regulates T cells' mitochondrial fitness to affect their survival, proliferation, and anti-tumor immune function.

T cells survival, proliferation, and anti-tumor response are closely linked to their mitochondrial health. Complement C1q binding protein (C1QBP) promotes mitochondrial fitness through regulation of mitochondrial metabolism and morphology. However, whether C1QBP regulates T cell survival, proliferation, and anti-tumor immune function remains unclear.

Taurine protects dopaminergic neurons in paraquat-induced Parkinson's disease mouse model through PI3K/Akt signaling pathways.

Taurine (Tau) is one of the most abundant amino acids in the brain and regulates physiological functions in the central nervous system, including anti-inflammatory effects. There is growing evidence that microglia-mediated neuro-inflammatory responses are an integral part of Parkinson's disease (PD) onset and progression. Among the many factors regulating the inflammatory response, phosphatidylinositol-3 kinase (PI3K) is susceptible to activation by a variety of cytokines and physicochemical factors, and subsequently recruits signaling proteins containing the pleckstrin homology structural domain to further regulate protein kinase B (AKT) expression involved in the regulation of the intracellular immune response and inflammatory response.

Sitagliptin activates the p62-Keap1-Nrf2 signalling pathway to alleviate oxidative stress and excessive autophagy in severe acute pancreatitis-related acute lung injury.

Acute lung injury (ALI) is a complication of severe acute pancreatitis (SAP). Sitagliptin (SIT) is a DPP4 inhibitor that exerts anti-inflammatory and antioxidant effects; however, its mechanism of action in SAP-ALI remains unclear. In this study, we investigated the effects of SIT on SAP-ALI and the specific pathways involved in SAP-induced lung inflammation, including oxidative stress, autophagy, and p62-Kelch-like ECH-associated protein 1 (Keap1)-NF-E2-related factor 2 (Nrf2) signalling pathways.

The prognostic value of sarcopenia combined with preoperative fibrinogen-albumin ratio in patients with intrahepatic cholangiocarcinoma after surgery: A multicenter, prospective study.

Background: To explore the prognostic value of the fibrinogen-albumin ratio (FAR) combined with sarcopenia in intrahepatic cholangiocarcinoma (ICC) patients after surgery and to develop a nomogram for predicting the survival of ICC patients.

Materials And Methods: In this prospective cohort study, 116 ICC patients who underwent radical surgery were enrolled as the discovery cohort and another independent cohort of 68 ICC patients was used as the validation cohort. Kaplan-Meier method was used to analyze prognosis.

Adoptive cell therapy of patient-derived renal cell carcinoma xenograft model with IL-15-induced γδT cells.

Adoptive transfer of γδ T cells is an attractive approach for cell-based immunotherapy in treatment of renal cell carcinoma (RCC). Interleukin-15 (IL-15) is the key physiological cytokine that regulates γδ T cell differentiation, proliferation and survival. In this work, we determined that IL-15 have the capacity to enhance the anti-tumoral functions of γδ T cells.

All-fiber mode-locked ytterbium-doped fiber laser with a saturable absorber based on the nonlinear Kerr beam cleanup effect.

We theoretically and experimentally demonstrate a novel, to the best of our knowledge, mode-locked ytterbium-doped fiber laser with a saturable absorber based on the nonlinear Kerr beam cleanup effect. The saturable absorber was formed by a 2-m graded-index multimode fiber, and a single-mode fiber segment served as a diaphragm. With an all-normal-dispersion-fiber configuration, the laser generated dissipative soliton pulses with pulse duration of 26.

lncRNA KCNQ1OT1 Suppresses the Inflammation and Proliferation of Vascular Smooth Muscle Cells through IκBa in Intimal Hyperplasia.

Inflammation and proliferation of vascular smooth muscle cells (VSMCs) are the key events in intimal hyperplasia. This study aimed to explore the mechanism by which long non-coding RNA (lncRNA) KCNQ1OT1 affects VSMC inflammation and proliferation in this context. A vein graft (VG) model was established in mice to introduce intimal hyperplasia.