Mechanism of the promotion of GEFS+ by the STAT3-mediated expression of interleukin-6.

Background: Genetic epilepsy with febrile seizures plus (GEFS+) is generally considered an ion channelopathy. To date, there have been few studies on inflammation associated with various types of epilepsy, and it remains unclear whether the inflammatory mechanism plays a key role in epilepsy.

Methods: In order to explore the role of the regulatory mechanism of immune factor expression in the pathogenesis of GEFS+, the present study detected the expression level of relevant immune factors such as interleukin-6 (IL-6) in peripheral blood of GEFS+ mice.

Mitochondrial tRNA mutations in Chinese Children with Tic Disorders.

Aims: To conduct the clinical, genetic and molecular characterization of 494 Han Chinese subjects with Tic disorders (TD).

Methods: In this study, we performed the mutational analysis of 22 mitochondrial tRNA genes in a large cohort of 494 Han Chinese subjects with TD via Sanger sequencing. These variants were then assessed for their pathogenic potential via phylogenetic, functional, and structural analyses.

Transient receptor potential melastatin 2 contributes to neuroinflammation and negatively regulates cognitive outcomes in a pilocarpine-induced mouse model of epilepsy.

Neuroinflammation contributes to the generation of epileptic seizures and is associate with neuropathology and comorbidities. Transient receptor potential melastatin 2 (TRPM2) expresses in various cell types in the brain. It plays a pathological role in a wide range of neuroinflammatory diseases, but has yet been studied in epilepsy.

TRPM2 ion channel is involved in the aggravation of cognitive impairment and down regulation of epilepsy threshold in pentylenetetrazole-induced kindling mice.

Epilepsy is one of the most common neurological conditions. Recent findings suggest that one of the mechanisms promoting its existence is calcium influx. The transient receptor potential melastatin type 2 channel (TRPM2) is a Ca-permeable cation channel that contributes to cell apoptosis; its possible signaling pathway is the PARP1/BNIP3/AIF/Endo G pathway that may be related to epilepsy.

TRPM2 channel regulates cytokines production in astrocytes and aggravates brain disorder during lipopolysaccharide-induced endotoxin sepsis.

Sepsis is one of the most significant challenges in intensive care units, which is associated with increased morbidity and mortality. Sepsis-associated encephalopathy (SAE) is a severe complication which can cause death and serious disabilities. Calcium signaling in astrocyte is essential for cellular activation and the potential resolution of infection or inflammation in SAE patients.