توجيهات نبوية لتعزيز المسؤولية الاجتماعية لدى الشباب

The role of youth in development of any society is vital. They are the vanguard of any nation. The youth cannot play their role properly and positively unless they understand their responsibilities fully. Creating sense of responsibility in individual of a society especially in its youth is inevitable for the collective and dynamic development of a society. The life of the holy Prophet (r) is a complete guide for all spheres of our life. It is evident from the teachings of the holy Prophet (r) and the general commandments of Islam that the youth play a very important role in socio economic and politico educational development. The holy Prophet (r) showed complete confidence in youth. He delegated them with different responsibilities, provided complete guidance and encouraged them for discharging their duties properly. The companions of the holy Prophet (r) who embraced Islam as a result of his first invitation were young between the ages of 20 to 30. The worst enemy of Islam- Abu Jahal was got killed by two young brothers. Likewise a young man Muṣ‘ab bin ‘Umayr (Ï) was sent to Madina, and Mu‘āz bin Jabal (Ï) and Abu Mūsá Ash‘arī (Ï) were sent to Yemen. Zayd bin Thābit (Ï) was directed to learn other languages. He also compiled the holy Qur’ān in Caliphate of Abū Bakar (Ï). The holy Prophet appointed Ḥuzayfa (Ï) to take census. For creating leadership characteristics, Usāmah bin Zayd was sent to different war expeditions. These are ample proofs of holy Prophet’s confidence he had in the youth.

Molecular Characterization of Familial Epilepsies

Epilepsy is an ailment of central nervous system that is characterized by inherent tendency of the brain to produce unprovoked seizures. Epilepsy could be idiopathic i.e.without a known cause (also cryptogenic) or symptomatic i.e. with a discernable clinical cause. Genetics play a crucial role in pathogenesis of both idiopathic and symptomatic epilepsies and molecular characterization holds prime importance and significance to delimit the genetic causes of the ailment. In the current study, five families (designated here as EP-01, EP-02, EP-03, EP-10 and EP-22) affected with idiopathic epilepsies were ascertained at molecular level through whole exome sequencing and Sanger sequencing to identify underlying genetic variants. The families EP-01 and EP-22 were affected with autosomal recessive progressive myoclonic epilepsy (also called Lafora disease). In family EP-01, we identified a novel missense variant c.262T>G in the EPM2A gene segregating with the disease phenotype. In silico analyses supported deleterious effects of the mutation by affecting the carbohydrate binding module of the EPM2A translated protein. In family EP-22, a recurrent nonsense variant c.793C>T in the NHLRC1 gene was identified as the likely cause of the disease phenotype in the family. The family EP-03 was affected with a Dravet-like phenotype. Whole exome sequencing identified a novel missense variant c.1342C>T in GRAMD1A gene. The variant was found segregating within the family in autosomal recessive mode and In silico analyses predicted deleterious effects of this variant on the protein function. Therefore, we suggest this novel GRAMD1A variant c.1342C>T identified in the current study as the likely cause of the epilepsy phenotype in the family EP-03. The involvement of GRAMD1A in epilepsy might be through involvement of endoplasmic reticulum - plasma membrane (ER-PM) transportation pathway. However, functional studies are required to explore the mechanism of pathogenesis. Families EP-02 and EP-10 were affected with autosomal dominant focal epilepsies. The family EP-02 presented with familial focal epilepsy with variable foci and the family EP-10 with lateral temporal lobe epilepsy. Both families were subjected to whole exome sequencing and the data were analyzed to find potential candidate variants that were tested for segregation in the affected families through Sanger sequencing. However, causative genetic variants were not identified in these families. Utilizing the standard Sanger sequencing and next generation sequencing technology (whole exome sequencing), we were able to find the likely cause of the disease in three Pakistani families affected with different epileptic pathologies at molecular level. These included a novel missense EPM2A variant, a recurrent nonsense NHLRC1 variant and a novel missense GRAMD1A variant. Two affected families were not resolved and warrant whole genome sequencing to unravel the genetic cause underlying epilepsy phenotype in these families. These data should be helpful in molecular diagnosis and screening of carriers in the affected families.