In addition, the Akt/mTOR signaling was found to be activated in rat hippocampus following FS, as evidenced by increased p-Akt and p-mTOR, while Fangjing decoction could inhibit the activation of Akt/mTOR signaling.
The specific inhibitor of TRPC3, Pyr3, remarkably attenuated the susceptibility and severity of seizures, neuronal cell death, and neuroinflammation in FS rats.
In this single-center, prospective, open, randomized controlled study, we included children and infants (age range: 6-60 months) with FSs who visited our hospital between May 1, 2015, and April 30, 2017.
Furthermore, the area under the ROC curve (AUC) of CSF MIG and IP-10 in distinguishing encephalitis from FC were 0.869 and 0.876, and the corresponding sensitivities/specificities were 67.7%/100.0% and 67.7%/95.5%, respectively.
Concomitantly, the apoptosis of hippocampal neurons, as well as Bax protein levels were also decreased in FS rats which were treated with Fangjing decoction.
The association of SNPs in PTGS2, in addition to IL6, IL-6 receptor (IL6R) and prostaglandin E receptor 3 (PTGER3) in prior reports, with FS suggests their possible action in concert to modulate phenotypes in FS as well as the involvement of thermoregulatory pathway in pathogenesis of FS.
To investigate possible association of FS with single nucleotide polymorphisms (SNPs) in prostaglandin-endoperoxide synthase-2 (prostaglandin G/H synthase-2; PTGS2/cyclooxygenase-2; COX2) gene involving in thermoregulatory pathway, eight SNPs, rs689465, rs689466, rs20417, rs13306038, rs201931599, rs689470, rs4648306 and rs4648308, along with 2 previously reported variations in IL1RN (86-bp VNTR) and IL10 (rs1900872) were genotyped and utilized for case-control association studies on 35 FS and 31 non-FS controls.
Using case-control genotypic association analysis, the -1192 A allele is most likely to confer susceptibility to FS by a recessive action model (p=0.045, pointwise empirical p value (EMP1)=0.049).
A genetic link between these two diseases is particularly evident in familial hemiplegic migraine: mutations of ATP1A2, SCN1A and CACNA1A genes, identified in this disease, have also been involved in different types of epilepsy and febrile seizures.
The association of SNPs in PTGS2, in addition to IL6, IL-6 receptor (IL6R) and prostaglandin E receptor 3 (PTGER3) in prior reports, with FS suggests their possible action in concert to modulate phenotypes in FS as well as the involvement of thermoregulatory pathway in pathogenesis of FS.
Calretinin (CR) -positive interneurons were transiently enhanced during epileptogenic period at 7-9 weeks after FS in the CA1 and DG region and it is double labeled with VGLUT-1.
A spectrophotometric assay was carried out to determine oxidative stress parameters (malondialdehyde, nitric oxide, reduced glutathione) and acetylcholinesterase activity in the cortex and hippocampus of FS and control animals.
Calretinin (CR) -positive interneurons were transiently enhanced during epileptogenic period at 7-9 weeks after FS in the CA1 and DG region and it is double labeled with VGLUT-1.
The association of SNPs in PTGS2, in addition to IL6, IL-6 receptor (IL6R) and prostaglandin E receptor 3 (PTGER3) in prior reports, with FS suggests their possible action in concert to modulate phenotypes in FS as well as the involvement of thermoregulatory pathway in pathogenesis of FS.
We detected higher levels of interleukin (IL)-1β and basic fibroblast growth factor (bFGF) in the cerebrospinal fluid (CFS) of patients with HHV-6B encephalitis when compared to those in patients with non-HHV-6B-induced febrile seizures.
Our study demonstrated that GluN2B phosphorylation at Tyr1472 site mediated by the transient increase of IL-1β was involved in the enhanced adult seizure susceptibility after prolonged FSs, implicating GluN2B-containing NMDAR is a new potential drug target with a wide therapeutic time window to prevent epileptogenesis in patients with infantile FSs.
Certain alleles, genotypes, and haplotypes in TGFB genes were over represented in patients with FS, which possibly could predispose individuals to this disease.