Early-Life Exposure to Paraquat Aggravates Sex-Specific and Progressive Abnormal Non-Motor Neurobehavior in Aged Mice.

Early-life exposure to environmental neurotoxicants is known to have lasting effects on organisms. In this study, we aim to investigate the impacts of PQ exposure during early developmental stages and adult re-challenge in aged mice on non-motor neurobehavior. Two mouse models, which were exposed once during early life stage and re-exposure at adulthood, were created to explore the long-term effects of PQ on non-motor neurobehavior.

Paraquat-induced neurogenesis abnormalities via Drp1-mediated mitochondrial fission.

Neurogenesis is a fundamental process in the development and plasticity of the nervous system, and its regulation is tightly linked to mitochondrial dynamics. Imbalanced mitochondrial dynamics can result in oxidative stress, which has been implicated in various neurological disorders. Paraquat (PQ), a commonly used agricultural chemical known to be neurotoxic, induces oxidative stress that can lead to mitochondrial fragmentation.

Toxicity of metal-based nanoparticles: Challenges in the nano era.

With the rapid progress of nanotechnology, various nanoparticles (NPs) have been applicated in our daily life. In the field of nanotechnology, metal-based NPs are an important component of engineered NPs, including metal and metal oxide NPs, with a variety of biomedical applications. However, the unique physicochemical properties of metal-based NPs confer not only promising biological effects but also pose unexpected toxic threats to human body at the same time.

Single-cell transcriptomic analysis reveals the adverse effects of cadmium on the trajectory of neuronal maturation.

Cadmium (Cd) is an extensively existing environmental pollutant that has neurotoxic effects. However, the molecular mechanism of Cd on neuronal maturation is unveiled. Single-cell RNA sequencing (scRNA-seq) has been widely used to uncover cellular heterogeneity and is a powerful tool to reconstruct the developmental trajectory of neurons.

Cadmium inhibits neural stem/progenitor cells proliferation via MitoROS-dependent AKT/GSK-3β/β-catenin signaling pathway.

Cadmium (Cd) is a toxic heavy metal widely found in the environment. Cd is also a potential neurotoxicant, and its exposure is associated with impairment of cognitive function. However, the underlying mechanisms by which Cd induces neurotoxicity are unclear.

Multiple Spontaneous Visceral Arterial Dissections in a Patient With Tolosa-Hunt Syndrome on Corticosteroid Therapy.

Multiple spontaneous visceral arterial dissections are an infrequent occurrence. The etiology, risk factors and natural history of these dissections have not been elucidated, and the optimal therapeutic strategy has not been established. We report a rare case of multiple spontaneous visceral arterial dissections involving the celiac artery, splenic artery, superior mesenteric artery, and right renal artery in a patient with Tolosa-Hunt syndrome on short-term corticosteroid therapy.

Single-cell RNA sequencing of mouse neural stem cell differentiation reveals adverse effects of cadmium on neurogenesis.

Cadmium (Cd) is a toxic heavy metal and widely exists in the environment. Extensive studies have revealed that Cd exposure can elicit neurotoxicity and potentially interfere with neurogenesis. However, underlying mechanisms by which Cd exposure affects neurogenesis remain unclear.

N-acetylcysteine alleviated paraquat-induced mitochondrial fragmentation and autophagy in primary murine neural progenitor cells.

The developing brain is uniquely vulnerable to toxic chemical exposures. Studies indicate that neural stem cell (NSC) self-renewal is susceptible to oxidative stress caused by xenobiotics. However, the impact of antioxidants on NSC self-renewal and the potential mechanisms remain elusive.

Modification of Wnt signaling pathway on paraquat-induced inhibition of neural progenitor cell proliferation.

Paraquat (PQ) is an agricultural chemical used worldwide. As a potential neurotoxicant, PQ adversely affects neurogenesis and inhibits proliferation of neural progenitor cells (NPCs). However, the molecular mechanistic insights of PQ exposure on NPCs remains to be determined.