Hepatic Steatosis Aggravates Vascular Calcification via Extracellular Vesicle-Mediated Osteochondrogenic Switch of Vascular Smooth Muscle Cells.

The global incidence of metabolic dysfunction-associated fatty liver disease (MAFLD) has risen sharply. This condition is strongly associated with the risk of cardiovascular disease (CVD), but how MAFLD affects the development and progression of CVD, particularly concerning vascular calcification, remains unclear. Herein, extracellular vesicles (EVs) are identified from steatotic hepatocytes as a trigger that accelerated the progression of both vascular intimal and medial calcification.

miR-32-5p induces hepatic steatosis and hyperlipidemia by triggering de novo lipogenesis.

Background And Objectives: MicroRNA-dependent regulation of hepatic lipid metabolism has been recognized recently as a key pathological mechanism contributing to the development of NAFLD. However, whether miR-32-5p (miR-32) plays a role in lipid metabolism or contributes to NAFLD remains unclear.

Methods And Results: A marked increase in miR-32 expression was observed in liver samples from patients and mice with NAFLD, as well as in palmitate-induced hepatocytes.

Serum MOTS-C Levels are Decreased in Obese Children and Associated with Vascular Endothelial Function.

Purpose: The increasing prevalence of obesity in children and its associated risk with cardiovascular diseases demand more discovery of the novel biomarkers for developing new treatment options for this complex disease. This study aimed to investigate the association of serum MOTS-C (a peptide encoded in the mitochondrial genome) levels and vascular endothelial function in obese children.

Patients And Methods: A total of 225 obese children (aged 8.

The ctDNA-based postoperative molecular residual disease status in different subtypes of early-stage breast cancer.

Background: Breast cancer is a highly heterogeneous disease. Early-stage, non-metastatic breast cancer is considered curable after definitive treatment. Early detection of tumor recurrence and metastasis through sensitive biomarkers is helpful for guiding clinical decision-making and early intervention in second-line treatment, which could improve patient prognosis and survival.

In Situ Inorganic Ligand Replenishment Enables Bandgap Stability in Mixed-Halide Perovskite Quantum Dot Solids.

Instability in mixed-halide perovskites (MHPs) is a key issue limiting perovskite solar cells and light-emitting diodes (LEDs). One form of instability arises during the processing of MHP quantum dots using an antisolvent to precipitate and purify the dots forming surface traps that lead to decreased luminescence, compromised colloidal stability, and emission broadening. Here, the introduction of inorganic ligands in the antisolvents used in dot purification is reported in order to overcome this problem.

All-Inorganic Quantum-Dot LEDs Based on a Phase-Stabilized α-CsPbI Perovskite.

The all-inorganic nature of CsPbI perovskites allows to enhance stability in perovskite devices. Research efforts have led to improved stability of the black phase in CsPbI films; however, these strategies-including strain and doping-are based on organic-ligand-capped perovskites, which prevent perovskites from forming the close-packed quantum dot (QD) solids necessary to achieve high charge and thermal transport. We developed an inorganic ligand exchange that leads to CsPbI QD films with superior phase stability and increased thermal transport.

Anatomic study of carpal tunnel in adults using monoenergetic reconstruction of dual-energy computed tomography.

Objective: To seek optimal keV settings for imaging carpal tunnel in adults by dual-energy computed tomography (DECT) monoenergetic technique; to describe anatomic characteristics of carpal tunnel and to observe correlation between carpal bony and soft tissue structures.

Methods: DECT images of 20 wrists (11 left and 9 right wrists; 14 men, mean age 26.93±1.

High Serum Asprosin Levels Are Associated with Presence of Metabolic Syndrome.

Objective: Asprosin, a new adipocytokine, has reportedly been associated with glucose release, dyslipidemia, and insulin resistance (IR). However, the relationship of asprosin with metabolic syndrome (MetS) remains unknown. This study aimed to investigate serum asprosin levels in MetS as well as their association with various metabolic parameters in humans.

ANXA1 Binds and Stabilizes EphA2 to Promote Nasopharyngeal Carcinoma Growth and Metastasis.

Overexpression of ANXA1 and EphA2 has been linked to various cancers and both proteins have attracted considerable attention for the development of new anticancer drugs. Here we report that ANXA1 competes with Cbl for binding EphA2 and increases its stability by inhibiting Cbl-mediated EphA2 ubiquitination and degradation in nasopharyngeal carcinoma (NPC). Binding of ANXA1 to EphA2 promoted NPC cell growth and metastasis and by elevating EphA2 levels and increasing activity of EphA2 oncogenic signaling (pS897-EphA2).

Betatrophin knockdown induces beiging and mitochondria biogenesis of white adipocytes.

Remodeling of energy-storing white fat into energy-consuming beige fat has led to a promising new approach to alleviate adiposity. Several studies have shown adipokines can induce white adipose tissue (WAT) beiging through autocrine or paracrine actions. Betatrophin, a novel adipokine, has been linked to energy expenditure and lipolysis but not clearly clarified.

[Level of circulating Alarin in obese children and its association with insulin resistance].

Objective: To study the level of circulating Alarin in obese children and its association with various metabolic parameters.

Methods: A total of 86 obese children with a body mass index (BMI) above the 95th percentile were enrolled as the obesity group, and 82 healthy children, matched for age and sex, with a BMI below the 85th percentile were enrolled as the healthy control group. According to the presence or absence of insulin resistance (IR), the obesity group was further divided into an IR group with 27 children and a non-IR group with 59 children.

Exogenous Hydrogen Sulfide Alleviates-Induced Intracellular Inflammation in HepG2 Cells.

Fatty acids induced hepatic inflammation plays an important role in nonalcoholic fatty liver disease (NAFLD) pathogenesis. Hydrogen sulfide (HS), an endogenous gasotransmitter, has been established to possess potent anti-inflammation in various human organs. However, the anti-inflammation property of HS in the fatty liver is still needed to further elucidate.

Serum CCN3 levels are increased in type 2 diabetes mellitus and associated with obesity, insulin resistance and inflammation.

Backgroud: CCN3 is a novel adipokine and has emerged as a potential metabolic regulator. However, information regarding the role of CCN3 in type 2 diabetes mellitus (T2DM) remains unclear. This study measured for the first time serum CCN3 levels in T2DM and explored the correlations between its serum levels and various metabolic parameters in humans.

S897 phosphorylation of EphA2 is indispensable for EphA2-dependent nasopharyngeal carcinoma cell invasion, metastasis and stem properties.

Our phosphoproteomics identified that phosphorylation of EphA2 at serine 897 (pS897-EphA2) was significantly upregulated in the high metastatic nasopharyngeal carcinoma (NPC) cells relative to non-metastatic NPC cells. However, the role and underlying mechanism of pS897-EphA2 in cancer metastasis and stem properties maintenance remain poorly understood. In this study, we established NPC cell lines with stable expression of exogenous EphA2 and EphA2-S897A using endogenous EphA2 knockdown cells, and observed that pS897-EphA2 maintained EphA2-dependent NPC cell in vitro migration and invasion, in vivo metastasis and cancer stem properties.

Zinc alpha2 glycoprotein protects against obesity-induced hepatic steatosis.

Background/aim: Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, impaired insulin sensitivity, and chronic low-grade inflammation. Our previous studies indicated that zinc alpha2 glycoprotein (ZAG) alleviates palmitate (PA)-induced intracellular lipid accumulation in hepatocytes. This study is to further characterize the roles of ZAG on the development of hepatic steatosis, insulin resistance (IR), and inflammation.

Photo-responsive camptothecin-based polymeric prodrug coated silver nanoparticles for drug release behaviour tracking via the nanomaterial surface energy transfer (NSET) effect.

A hybrid drug delivery system was successfully fabricated by attaching a camptothecin (CPT)-based polymeric prodrug onto the surface of silver nanoparticles (AgNPs). PEG was employed as a macro-RAFT agent in RAFT polymerization to synthesize a branched star copolymer, to which CPT is linked through the photo-responsive o-nitrobenzyl linkage. In vitro tests indicate that the fluorescence of CPT in the polymeric prodrug is quenched by AgNPs based on the nanomaterial surface energy transfer (NSET) effect and the fluorescence recovers when the CPT molecules are released from hybrid nanoparticles.

MiR-125b regulates proliferation and apoptosis of nasopharyngeal carcinoma by targeting A20/NF-κB signaling pathway.

MiR-125b is aberrantly expressed and has a role in the various types of tumors. However, the role and mechanism of miR-125b in nasopharyngeal carcinoma (NPC) are unclear. In this study, we investigated the role and mechanism of miR-125b in NPC.

MiR-23a sensitizes nasopharyngeal carcinoma to irradiation by targeting IL-8/Stat3 pathway.

Radioresistance poses a major challenge in nasopharyngeal carcinoma (NPC) treatment, but little is known about how miRNA regulates this phenomenon. In this study, we investigated the function and mechanism of miR-23a in NPC radioresistance, one of downregulated miRNAs in the radioresistant NPC cells identified by our previous microarray analysis. We observed that miR-23a was frequently downregulated in the radioresistant NPC tissues, and its decrement correlated with NPC radioresistance and poor patient survival, and was an independent predictor for reduced patient survival.

MiRNA-203 Reduces Nasopharyngeal Carcinoma Radioresistance by Targeting IL8/AKT Signaling.

Radioresistance poses a major challenge in nasopharyngeal carcinoma (NPC) treatment, but little is known about how miRNA (miR) regulates this phenomenon. In this study, we investigated the function and mechanism of miR-203 in NPC radioresistance, one of downregulated miRs in the radioresistant NPC cells identified by our previous microarray analysis. We observed that miR-203 was frequently downregulated in the radioresistant NPC tissues compared with radiosensitive NPC tissues, and its decrement significantly correlated with NPC radioresistance and poor patient survival, and was an independent predictor for reduced patient survival.

Reduction of RKIP expression promotes nasopharyngeal carcinoma invasion and metastasis by activating Stat3 signaling.

The role and underlying mechanism of Raf kinase inhibitory protein (RKIP) in nasopharyngeal carcinoma (NPC) metastasis remain unclear. Here, we showed that RKIP was downregulated in the NPC with high metastatic potentials, and its decrement correlated with NPC metastasis and poor patient survival, and was an independent predictor for reduced overall survival. With a combination of loss-of-function and gain-of-function approaches, we observed that high expression of RKIP reduced invasion, metastasis and epithelial to mesenchymal transition (EMT) marker alternations of NPC cells.