This study demonstrated the significance of anti-IL-1β-mAb treatment in acute TLE with respect to the unique advantages of SPIONs and the active location-targeting characteristic of AMT.
In summary, this study shows that enhancive miR-146a can upregulate the inflammatory factor IL-1β in chronic TLE by downregulating CFH, and that upregulation of IL-1β plays an important feedback-regulating role in the expression of miR-146a and CFH, forming a miR-146a-CFH-IL-1β loop circuit that initiates a cascade of inflammation and then leads to the perpetuate inflammation in TLE.
We investigated Kir4.1 (Kcnj10) and IL-1β mRNA expression in the temporal cortex in a rat model of temporal lobe epilepsy 24 h and 1 week after induction of status epilepticus (SE), using real-time PCR and western blot analysis.
The objective of this study is to replicate previously published results regarding the involvement of several susceptibility genes in temporal lobe epilepsy (TLE): interleukin 1beta (IL-1beta), interleukin 1beta (IL-1alpha), interleukin 1RA (IL-1RA), apolipoprotein E (ApoE) and prodynorphin (PDYN).
The results show a modest association (OR, 1.48; 95% confidence interval, 1.09-2.00; P = 0.01) between the IL-1 beta-511T polymorphism and temporal lobe epilepsy with hippocampal sclerosis.
The results show a modest association (OR, 1.48; 95% confidence interval, 1.09-2.00; P = 0.01) between the IL-1 beta-511T polymorphism and temporal lobe epilepsy with hippocampal sclerosis.
In a recent study, patients with temporal lobe epilepsy were reported to carry the interleukin-1beta allele 2 at position -511 more often than healthy control subjects.
To elucidate a genetic predisposition of temporal lobe epilepsy with hippocampal sclerosis (TLE-HS+), we studied polymorphisms in the IL-1beta, IL-1alpha, and IL-1 receptor antagonist (IL-1RA) genes in 50 patients with TLE-HS+ and in 112 controls.