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العنوان
study of the relation between long non-coding ribonucleic acid snhg16 and vitamin d status in juvenile myoclonic epilepsy egyptian patients/
المؤلف
Moustafa, Salma Sabry Gomaa.
هيئة الاعداد
باحث / سلمى صبري جمعة مصطفى
مشرف / سعد الدين عبد الفتاح أبو النعمان
مشرف / أيمن عبده برغش
مشرف / إيمان سليمان قمحة
الموضوع
Medical Biochemistry.
تاريخ النشر
2022.
عدد الصفحات
P63. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب
تاريخ الإجازة
25/6/2022
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Medical Biochemistry
الفهرس
Only 14 pages are availabe for public view

from 80

from 80

Abstract

Epilepsy is a neurological disease characterized by recurring unprovoked seizures which seriously affect the daily activities and the physical and mental health of epileptic patients. Epilepsy affects people of all ages, races, and social classes.
Many hypotheses have been postulated recently to explain the aetiopathogenesis of epilepsy, including neuroinflammation, oxidative stress, hypoxia, disruption of the glutamatergic system and other chemical mediators, dysregulation of the BBB, and DNA epigenetic alterations.
Despite the considerable progress in clinical and preclinical epilepsy research, the pathophysiology of epilepsy remains an open question.
LncRNAs regulate the gene expression of pro-inflammatory and anti-inflammatory cytokines in the CNS. SNHG16 has been shown to counteract the inflammatory response and reduce hydrogen peroxide-induced toxicity.
Several studies suggest that vitamin D3 supplementation raises the threshold of chemically induced seizures and suppresses epileptic activity by reducing the expression of certain proconvulsant cytokines.
In the present study, the aim was to study the relation between SNHG16 and vitamin D3 status in JME Egyptian patients.
To achieve this aim, 45 individuals were included in the study and they were divided into the following groups:
group I: included 15 JME patients on valproate therapy.
group II: included 15 newly diagnosed JME patients who didn’t receive any antiepileptic treatment before.
group III: included 15 healthy age- and sex-matched volunteers as a control group.
The following investigations were performed for all patients and healthy subjects:
• Total RNA was extracted from serum samples followed by RT real-time PCR. Then the expression of serum SNHG16 was calculated using the comparative cycle threshold approach (2–ΔΔCT).
• Serum 25-hydroxy vitamin D3 levels were measured using a commercially available ELISA kit.
Statistical analysis of the studied parameters showed that:
• Serum levels of SNHG16 relative expr