A psychological education model integrating artificial intelligence-based BERT in physical education.

Epilepsy is among the most common chronic neurological disorders and affects approximately 70 million people worldwide. Although more than 30 antiseizure medications are currently available, approximately one-third of patients fail to achieve sustained seizure freedom with at least two appropriately selected, well-tolerated drugs and consequently develop drug-resistant epilepsy. Recurrent seizures not only lead to severe physical injuries—falls, burns, fractures, and asphyxia—but also give rise to psychiatric comorbidities (depression and anxiety) and impose substantial social and economic burdens. The hippocampus plays a pivotal role in epileptogenesis. Hippocampal sclerosis, characterised by selective neuronal loss, axonal sprouting, synaptic reorganisation, and structural/functional alterations of glial cells, is the most frequent pathological finding in patients with epilepsy. Postoperative tissue analyses revealed hippocampal sclerosis in 36.4% of patients, 61.4% of whom remained seizure free one year after lesionectomy. High-resolution MRI has demonstrated hippocampal atrophy in nearly all individuals with refractory epilepsy. Similarly, in pilocarpine-induced status epilepticus (SE) models, extensive hippocampal neuronal loss and robust glial proliferation are consistently observed. This study employed the pilocarpine model—the standard and most widely used chemoconvulsant protocol for temporal lobe epilepsy (TLE)—to validate and extend recent single-cell, single-nucleus, and xenium-based spatial transcriptomics findings obtained in the kainic acid (KA) model. Although pilocarpine (a muscarinic receptor agonist) and kainic acid (a glutamatergic excitotoxin) induce status epilepticus through distinct primary mechanisms, both reliably recapitulate the hippocampal sclerosis, spontaneous recurrent seizures, and epileptogenic remodelling observed in human drug-resistant TLE. We hypothesized that cell type-specific transcriptional changes would reveal conserved epileptogenic mechanisms across models, while potentially identifying pilocarpine-specific features. This comparative framework enhances the generalizability of our findings, rendering them less susceptible to model-specific artifacts.