Almighty Allah revealed the Holy Qur’an for guidance of the mankind. This guidance cannot be acquired without pondering over the meanings of this book. Different scholars dedicated their lives for understanding and then spreading the message of the Almighty Allah. This book is a study of the work on translations and tafasīr of Holy Qur’an. In Sub-Continent, a large number of religious scholars dedicated themselves for the service of Holy Qur’an. Their vision was broad and they elaborated meanings of the Holy Qur’an according to their own mental approach They were appreciated and criticized by scholars of different sects of the society. There is a dire need to understand and spread the teachings of the Holy book. Hopefully this work will encourage the readers to be aware of the research of theologians. Shāh Walī Allāh is the most important religious figure of Sub-Continent. He and his sons played very important role in spreading the message of Qur’an. Brief services of this family are elaborated in this book. Scholars of Sindh have contributed in writing translations and commentaries of Holy Qur’an. Some of their contributions are highlighted. The reader will also find introduction of well-known translations and tafasīr of the 20th century. But this introduction is restricted to the Sub-continent. Through this book. the writer wants only to motivate people for learning the Holy Book. It is not claimed that services of all the Qur’anic theologians of Sub-continent are highlighted. This is a matter of pride for the author that things are discussed without any prejudice. The readers are the best judges. Suggestions regarding the improvement will be welcomed. I am thankful to Prof. Dr. Shams-ul-Basar and Dr. Zohaib Ahmad for guidance and Co-operation regarding the publication of this work. May Allah Almighty shower blessings on them. If...
Communication development has made the world a global village. The modern and art education is lasting in this era. Due to this interacting atmosphere of epistemic collaboration takes place. Hence, only international seminars and interfaith dialogues are considered to be the meaningful. Quran as the root source of seerah explained by various interpreters according to their knowledge taste. Imam addalji (died 947 A.H) also interpreted verses of seerah as well as “al-Shifa̅” text in his famous manuscript (“al-Istif a̅’ libaya̅n Ma ̒ a̅ni̅ al-Shifa̅”) in pure cognitive contents. The following research paper reviews the discussions of cognitive contents described under the interpretation of ayat al majeah and rahmat in his Manuscript. The main objective is to focus the reality that Quran is not against the art education in Fact Quran in itself has a very deep educational and artistic values. They can please the research keenness of human intellectual capacity in best way.
In human, genetic disorders of the nails are very rare and occur in both isolated and syndromic form. In syndromic forms, anomalies in other ectodermal appendages and/or skeletal deformities are associated with nail disorders. Over the past few years several, different types of human nail disorders have been characterized at clinical and molecular levels. In few cases of nail disorders, causative genes have been identified. In the study presented in the dissertation, eight Pakistani families (A-H) representing isolated form of nail dysplasia (Families A-F) and syndromic nail disorders (Families G and H) have been characterized both at clinical and molecular levels. Family A showed autosomal recessive isolated congenital fingernail dysplasia. Whole exome sequencing of the family revealed a novel variant c.92G>T (p.Arg31Leu; MAF=0.0001; chr10:70,287,041) in the SLC25A16 (NM__152707.4) gene. Affected individuals in two families, B and C, showed typical phenotypes of hereditary leukonychia. Based on the phenotypes observed the PLCD1 gene was sequenced in all available individuals of both families. Analysis of sequencing data showed a recurrent heterozygous mutation c.625T>C (p.Cys209Arg; MAF=0.00009; chr3: 38,052,933) in family B. In family C analysis of sequencing data did not reveal any mutation in PLCD1 (NM_001130964.1) gene. To ascertain the causative gene, the DNA sample of an affected family member has been submitted for exome sequencing. In two other families (D and E) of isolated nail dysplasia, linkage was established to mapped on chromosome 8q22.3. Subsequent sequencing of the FZD6 (NM_003506.4) gene revealed a homozygous non-sense variant c.1750G>T (p.E584X*; MAF=0.00001; chr8:104,342,091) in family D and a homozygous missense variant c.1266G>A ( p.Gly422Asp; MAF=0.00001; chr8:104,342,091) in family E. In family F the nails of Genetic Analysis of Human Hereditary Nail Dysplasia in Pakistani Families the affected individuals were thick and hard with deformed nail bed. After failing to establish linkage to the known genes in the family, DNA samples were used for SNP microarray genotyping. This identified four homozygous regions. To identify a causative gene in the linked regions, DNA sample of an affected individual has been submitted to exome sequencing. In family G, affected individuals displayed typical phenotypes of pure hair and nail ectodermal dysplasia. All affected individuals of the family showed homozygosity with several markers related to HOXC13 (NM_017410.3) gene at chromosome 12p11.1- q21.1. Sequence analysis of HOXC13 revealed a novel homozygous missense mutation c.929A>C (p.Asn310Thr; chr12: 54,338,976). Family H segregated autosomal recessive form of primary hypertrophic osteoarthropathy. Homozygosity mapping, based on whole genome SNP genotyping, lead to the identification of 7.05 Mb homozygous region at chromosome 4q34.1-q34.3. The HPGD (NM_000860.6) gene, located in the homozygous region, was sequenced which detected a homozygous missense variant c.577T>C (p.S193P; chr4: 175,414,387) in all affected family members. The study presented here involves the clinical and genetic analysis of eight families collected from different remote areas of Pakistan. Six of them were characterized by isolated congenital nail dysplasia while two others with syndromic nail disorders. In these families mutation analysis of SLC25A16, PLCD1, FZD6, HOXC13 and HPGD genes revealed some novel and recurrent mutations. In addition, failure to establish linkage to known genes in two families (C and F) directed the existence of undiscovered genes in the human genome triggering nail dysplasia phenotypes.