BDE-47 induces metabolic dysfunction-associated steatotic liver disease (MASLD) through CD36-mediated increased fatty acid uptake and PPARα-induced abnormal fatty acid oxidation in BALB/c mice.

The widespread existence of 2,2',4,4'-tetra-bromodiphenyl ether (BDE-47) in the environment has aroused great concern. BDE-47 induces the occurrence of metabolic dysfunction-associated steatotic liver disease (MASLD), but the mechanism has not been fully elucidated. Here, we further investigate the underlying mechanism using BALB/c mice.

Neuroprotective Roles of Apelin-13 in Neurological Diseases.

Apelin is a natural ligand for the G protein-coupled receptor APJ, and the apelin/APJ system is widely distributed in vivo. Among the apelin family, apelin-13 is the major apelin isoform in the central nervous system and cardiovascular system, and is involved in the regulation of various physiopathological mechanisms such as apoptosis, neuroinflammation, angiogenesis, and oxidative stress. Apelin is currently being extensively studied in the nervous system, and apelin-13 has been shown to be associated with the onset and progression of a variety of neurological disorders, including stroke, neurodegenerative diseases, epilepsy, spinal cord injury (SCI), and psychiatric diseases.

Differential effects of PEGylated Cd-free CuInS/ZnS quantum dot (QDs) on substance P and LL-37 induced human mast cell activation.

CuInS/ZnS-PEG quantum dots (QDs) are among the most widely used near infrared non-cadmium QDs and are favored because of their non-cadmium content and strong tissue penetration. However, with their increasing use, there is great concern about whether exposure to QDs is potentially risky to the environment and humans. Furthermore, toxicological data related to CuInS/ZnS-PEG QDs are scarce.

BDE-47 disturbs the immune response of lymphocytes to LPS by downregulating NF-κB pathway.

The health risks associated with 2,2',4,4'-tetra-bromodiphenyl ether (BDE-47) have become an increasing concern due to its widespread presence in the environment and biological samples. To date, the potential toxicity of BDE-47 to immune system remains unclear. In this study, we aimed to study the immunotoxicity of BDE-47 using spleen-derived lymphocytes in vitro and BALB/c mice in vivo.

BDE-47 induced PC-12 cell differentiation via TrkA downstream pathways and caused the loss of hippocampal neurons in BALB/c mice.

As the most abundant congener of polybrominated diphenyl ethers (PBDEs) detected in environment and human biotic samples, 2, 2', 4, 4'-tetrabromodiphenyl ether (BDE-47) has been found to accumulate in brain and induce neurotoxicity, however, the detailed mechanism has not been clearly elucidated. To investigate the neurotoxicity of BDE-47, undifferentiated PC-12 cells were exposed to different doses of BDE-47, and BDE-47 dissolved in corn oil was orally administered to mice for 8 consecutive weeks. Our data showed that BDE-47 obviously changed cell morphology, altered cell viability, promoted cell apoptosis, and induced reactive oxygen species (ROS) production.

Retrospective analysis of changes in the anterior corneal surface after Q value guided LASIK and LASEK in high myopic astigmatism for 3 years.

Background: To compare the corneal high-order aberrations (HOAs), asphericity and regularity after Q-value guided laser in situ keratomileusis (LASIK) and laser epithelial keratomileusis (LASEK) in high myopic astigmatism.

Methods: In this retrospectively comparative study, we measured the corneal HOAs, asphericity indices (Q values) and corneal regularity indices preoperatively and 36 months postoperatively in 70 eyes (35 patients) with Q-value guided surgeries. All the patients with high myopic astigmatism were divided into two groups which included 34 eyes underwent LASIK and 36 eyes underwent LASEK procedures.