Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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UNKNOWN
80 participants
OBSERVATIONAL
2020-02-01
2020-12-01
Brief Summary
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Experimental studies and clinical evidence obtained in animal models of epilepsy and human brain specimen from various drug-resistant forms of epilepsy show the activation of the innate and adaptive immunity mechanisms and the induction of the associated inflammatory processes in the epileptogenic foci.
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Detailed Description
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There is a clear cause for epilepsy in only a minority of the cases, while in up to70% of all case of epilepsy in adults and children, no cause can be discovered. Some of the main causes of epilepsy include: Low oxygen during birth, head injuries that occur during birth or from accidents during youth or adulthood, brain tumors, infections such as meningitis or encephalitis, stroke or any other type of damage to the brain.
A role of inflammatory molecules in the generation of seizures had been first investigated when selected anti-inflammatory treatments, in particular, steroids, immuno-globulins, and adrenocorticotropic hormone (ACTH), were shown to control seizures in pediatric epilepsies refractory to conventional anticonvulsive drugs. In addition, specific epileptic disorders have been associated with the presence of neuronal antigen-directed antibodies in plasma or cerebrospinal fluid (CSF).
A nucleotide-binding oligomerization domains (NODs) are cytosolic proteins that include key regulators of apoptosis and pathogen resistance in mammals and plants. A large number of NODs contain leucine-rich repeats (LRRs), hence referred to as NOD-LRR proteins. The NLRP3 gene provides instructions for making a protein called cryopyrin. Cryopyrin is a member of a family of proteins called nucleotide-binding domain and leucine-rich repeat containing (NLR) proteins. NLR family have two common features: the first is a nucleotide-binding oligomerization domain which is bound by ribonucleotide-phosphates (rNTP) and is important for self-oligomerization. The second is a C-terminal leucine-rich repeat, which serves as a ligand-recognition domain for other receptors (e.g. Toll like receptor (TLR)) or microbial ligands, while NLRP3 has been identified in microglial cells.
Conditions
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Study Design
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CASE_CONTROL
CROSS_SECTIONAL
Study Groups
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epileptic children
fifty patient with epilepsy
Expression of nucleotide protein -3
Expression of nucleotide protein -3 will be measured in serum by ELISA
Healthy controls
thirty healthy control
Expression of nucleotide protein -3
Expression of nucleotide protein -3 will be measured in serum by ELISA
Interventions
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Expression of nucleotide protein -3
Expression of nucleotide protein -3 will be measured in serum by ELISA
Eligibility Criteria
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Inclusion Criteria
Exclusion Criteria
* patient who have apparent infection
2 Years
17 Years
ALL
No
Sponsors
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Assiut University
OTHER
Responsible Party
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Reham I El-mahdy
Principal Investigator
Central Contacts
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References
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He Q, Jiang L, Man S, Wu L, Hu Y, Chen W. Curcumin Reduces Neuronal Loss and Inhibits the NLRP3 Inflammasome Activation in an Epileptic Rat Model. Curr Neurovasc Res. 2018;15(3):186-192. doi: 10.2174/1567202615666180731100224.
Farghaly WM, Abd Elhamed MA, Hassan EM, Soliman WT, Yhia MA, Hamdy NA. Prevalence of childhood and adolescence epilepsy in Upper Egypt (desert areas). Egypt J Neurol Psychiatr Neurosurg. 2018;54(1):34. doi: 10.1186/s41983-018-0032-0. Epub 2018 Nov 9.
Xu D, Miller SD, Koh S. Immune mechanisms in epileptogenesis. Front Cell Neurosci. 2013 Nov 8;7:195. doi: 10.3389/fncel.2013.00195. eCollection 2013.
Other Identifiers
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Epilepsy
Identifier Type: -
Identifier Source: org_study_id
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