Nocturnal enuresis in children: Parents' perspectives.

AIM: Parents of children with nocturnal enuresis (NE) may have uncertainty and anxiety. This study aimed to investigate the level of uncertainty and anxiety in the parents of children with NE and analyse its influencing factors. DESIGN: We conducted a descriptive cross-sectional study among the parents of children with NE in China. METHODS: A general information questionnaire, the Parent Perception of Uncertainty Scale (PPUS), and the Self-Rating Anxiety Scale (SAS) were used. Multiple linear regression analysis was used to identify factors influencing the parental uncertainty level independently. RESULTS: A total of 247 valid questionnaires were collected. The PPUS score of children with NE was 81.18 ± 10.82, and the anxiety self-rating scale score was 41.86 ± 9.20. Parents' working status, the family's per capita monthly income, and the children's treatment time were the main influencing factors of parental illness uncertainty.

Expression of SOCSs and TLRs in the hippocampus of pentylenetetrazole kindling model.

BACKGROUND: Epilepsy is one of the most common neurological disorders, and approximately one-third of patients with epilepsy are resistant to anti-epileptic drugs (AEDs). Recent emerging evidence has demonstrated the roles of innate immunity and the associated inflammatory processes in epilepsy. Toll-like receptors (TLRs) are a type of pattern-recognition receptor that promote innate immune defense. The SOCS proteins as negative-feedback regulators in cytokine signaling are involved in the regulation of TLR-mediated immune responses. However, few studies investigating the role of TLRs and SOCSs in epilepsy have been reported. METHODS: To explore the role of innate immunity in the mechanism of epilepsy, the pentylenetetrazole (PTZ) kindling rat model was established using intraperitoneal injection of PTZ. The expression levels of TLR2, TLR4, and STAT molecules in rat hippocampi were analyzed using qRT-PCR and western blotting techniques. The expression levels of SOCS-1 and SOCS-3 in rat hippocampi were analyzed using qRT-PCR. RESULTS: Our data demonstrated that both the mRNA and protein expression of TLR2 and TLR4 were significantly upregulated in the rat hippocampus with PTZ injection, which was accompanied by an inhibition of SOCS-1 and SOCS-3 and an upregulation of STAT3. CONCLUSIONS: Our study suggested that SOCSs and TLRs contribute to the development of epilepsy which may lead to therapeutic interventions that limit epileptogenesis.

GSK-3ß may be involved in hippocampal mossy fiber sprouting in the pentylenetetrazole-kindling model.

Mossy fiber sprouting (MFS) is a pathological phenomenon that is commonly observed in temporal lobe epilepsy (TLE). However, the molecular mechanisms underlying MFS remain unclear. It has been demonstrated that the tau protein is important in the progression of MFS by the regulation of microtubule dynamics and axonal transport, with all of these functions of tau modulated by its site-specific phosphorylation. Glycogen synthase kinase-3ß (GSK-3ß) is an active kinase that regulates the phosphorylation of tau protein. Therefore, it was hypothesized that GSK-3ß contributes to MFS by phosphorylating tau protein. The aim of the present study was to determine the expression and activity of GSK-3ß at different regions in the rat hippocampus during the pentylenetetrazole (PTZ)-kindling process in order to demonstrate the possible correlation with MFS, and to investigate the involvement of GSK-3ß in epileptogenesis. Male Sprague-Dawley rats (n=180) were randomly divided into the control and PTZ-treated groups. The chronic epileptic model was established by intraperitoneal injection of PTZ and the hippocampus was observed for the presence of MFS using Timm staining. GSK-3ß mRNA, protein and activity were analyzed in various regions of the hippocampus using in situ hybridization, immunohistochemistry and immunoprecipitation followed by a kinase assay and liquid scintillation counting, respectively. MFS was observed prior to kindling and an increased distribution of Timm granules were observed in the CA3 region of the PTZ-treated rats; however, this was not demonstrated in the supragranular layer of the dentate gyrus. The expression of GSK-3ß mRNA and protein, as well as the GSK-3ß activity, increased significantly from 3 days to 4 weeks in the PTZ group, and this was correlated with the progression of MFS in the CA3 area. In addition, it was demonstrated that MFS did not result from TLE. GSK-3ß may therefore be involved in the progression of MFS and is important in epileptogenesis. An understanding of the molecular mechanisms underlying MFS may lead to the identification of a novel therapeutic target to limit epileptogenesis.

Potential roles of Cdk5/p35 and tau protein in hippocampal mossy fiber sprouting in the PTZ kindling model.

BACKGROUND: The most well-documented synaptic reorganization associated with temporal lobe epilepsy is mossy fiber sprouting (MFS), which is believed to play a critical role in epileptogenesis. However, the molecular mechanisms underlying this phenomenon remain unclear. Cyclin-dependent kinase 5 (Cdk5) is a proline-directed serine/threonine kinase which is found to be crucial in axon growth and synaptic plasticity. We hypothesized that Cdk5 contributed to MFS via phosphorylating its substrate tau protein, which was known to facilitate microtubule stabilization and axonal elongation. METHODS: 240 male SD rats were randomly divided into the control group and PTZ group. The epileptic models were established by intraperitoneal PTZ injection, while the control rats were injected with an equal dose of saline. At different time points, Cdk5/p35 mRNA and protein, total tau protein and its phosphorylation at Ser202 (p-tau) and Cdk5 activity were analyzed in different regions of hippocampus by in situ hybridization, immunohistochemistry, Western blot, immuno-precipitation and liquid scintillation counter. Hippocampus was also evaluated for MFS with Timm stain. RESULTS: Prominent MFS was observed in area CA3 rather than the inner molecular layer in PTZ treated rats and the degree of MFS progressed with the development of behavioral kindled seizures. The expression of Cdk5/p35 mRNA and protein, tau protein and its phosphorylation at Ser202 significantly increased from 3 days to 4 weeks in the PTZ group, which was in accordance with the progression of MFS in area CA3. CONCLUSIONS: Cdk5/p35 and its substrate tau protein may be involved in MFS. Understanding the molecular mechanisms underlying MFS may lead to therapeutic interventions that limit epileptogenesis.

Mossy fiber sprouting, hippocampal damage and spontaneous recurrent seizures in pentylenetetrazole kindling rat model.

AIM: The aim of this study was to determine the correlations among hippocampal damage, spontaneous recurrent seizures (SRS), and mossy fiber sprouting (MFS) using pentylenetetrazole (PTZ) kindling model. METHODS: Chronic epileptic model was established by administration of PTZ. Behaviour and EEG seizure activity were recorded. Rats' hippocampus were analyzed with haematoxylin and eosin (H&E) stain for histological lesions and evaluated for MFS with Timm stain. RESULTS: Prominent MFS was observed in area CA3 rather than the inner molecular layer in PTZ treated rats and the degree of MFS progressed with the development of behavioral kindled seizures. MFS preceded the occurrence of spontaneous seizures. No obvious neuronal necrosis and loss were observed in different regions of the hippocampus during kindling progression. CONCLUSION: MFS is not the outcome of SRS. Severe hippocampal damage is not required in the development of MFS and SRS.