مولانا محمد جلیل کیرانوی
افسوس ہے کہ گزشتہ ماہ اگست میں حضرت شیخ الہندؒ کے دومنتسبین،مولانا محمد جلیل کیرانوی استاذ اورمولانا محمد مبارک علی نائب مہتمم دارالعلوم دیوبند واصل بحق ہوکر اس جہانِ فانی کوالوداع کہہ گئے۔اناﷲ وانا الیہ راجعون۔ اوّل الذکر (المتولد۱۳۱۸ھ)نے اگرچہ دورۂ حدیث حضرت الاستاذ مولانا محمد انورشاہ کے عہد میں تمام کیا تھا لیکن درحقیقت پروردہ تھے حضرت شیخ الہند کے گھرانے کے ہی۔ نوبرس کی عمر تھی کہ اُن کے والد حضرت ؒ کے سپردکرگئے تھے۔یہ اس آستانۂ قدس کوایسے چمٹے کہ مرتے دم تک اسے نہ چھوڑا۔اس لیے حضرت شیخ الہند کے خادم خاص اور شریکِ جلوت وخلوت تھے اس بناء پر حضرت شیخ الہند کی مشہور’’ریشمی خطوط‘‘والی تحریک کے جزوکل سے خوب واقف اوراس کے محرمِ اسرار تھے۔اس سلسلہ میں انھوں نے بڑے بڑے مصائب اورشدائد برداشت کئے لیکن تحریک کابھید آشکار نہیں کیا۔حضرت ؒ کی وفات کے بعد ادہر ادہرمدرس رہے۔آخر میں دیوبند آگئے تھے اوردرس کی خدمات انجام دیتے تھے۔
[ستمبر۱۹۶۸ء]
Islam lays emphasis on social justice and sharing of resources between the haves and the have-nots. In order to create such a balanced socio-economic environment, the inter-class lending is considered to be a way forward ethical activity. Qard is a gratuitous contract in which one gives a certain homogeneous wealth to other against the condition of returning of similar value of wealth upon demand or after termination of payback period. As per Sharia'h, the Qard should not bring any return or benefit for the lender because that would be equivalent to Ribâ. Therefore the lender cannot charge or demand any extra amount against the extension on the payback period awarded to the poor borrower. Furthermore, Islam considers the difference between debtors who default by procrastination and those who default by necessity. The Holy Qur'an, in principal, recommends having compassion for the poor barrowers and giving them the grace period till they have the capacity to payback. In such scenario the Muslim lenders perceive that the Islam has set unilateral direction in favor of borrowers only. Therefore the lenders feel that they are handicapped or helpless and found themselves in a strangled situation. This study is designed to solve the dilemma of lenders and explore risk mitigation strategies in case of insolvency of borrowers. The verses from the Holy Qur'an & Hadith of the Messenger (PBUH) and also work of prominent Sharia'h Scholars were considered to form a comprehensive guideline to mitigate the lender’s risk. Hence it has been proved that the Islam has given legal rights to the lender and allows some practical recovery strategies & tactics to recover the funds from the underprivileged borrowers. This study will play a key role in risk mitigation for default and late payments.
Genetic defects in the complex processes of embryonic development of the skeleton and its postnatal maintenance result in different types of clinically diverse and genetically heterogeneous skeletal disorders. This presents a diagnostic challenge because of their nonspecific presentation, variable clinical features, highly overlapping phenotypes and lack of recognition as a discrete clinical entity. The research work, presented in this dissertation, describes clinical and molecular investigations of fourteen families (A-N) segregating various forms of skeletal disorders in autosomal recessive pattern. Clinical examinations were performed at local Government hospitals. Blood samples were collected from both affected and unaffected members of the families. Genomic DNA, extracted from the blood samples, was used for microsatellite and SNP based genetic mapping and whole exome and chain termination sequencing. Clinical features, observed in affected members of six families (A-F), were analogous to a condition named as mucopolysaccharidosis. Linkage in these families was established to chromosome 16q24.3 harboring GALNS gene. Sanger sequencing revealed two novels (p.Phe216Ser, p.Glu121Argfs*37) and two previously reported mutations (p.Pro420Arg, p.Arg386Cys) in GALNS gene in the six families. In silico analysis predicted that the missense mutations affect structure and function of the GALNS protein. Clinical and radiographic examinations of affected members in three families (G-I) underscored the manifestations of acromesomelic dysplasia. Microsatellite based genotyping followed by sequence analysis of the NPR2 gene identified three novel missense mutations (p.Arg749Trp, p.Arg601Ser, p.Leu314Arg) in the families. Human genome scan using SNP microarray followed by exome sequencing discovered a potentially casual frameshift mutation (c.594-595insT; p.Gln198Thrfs*21) in a novel gene KIAA0825 in the family J segregating post-axial polydactyly in an autosomal recessive manner. Affected individuals in family K exhibited peculiar clinical features including post axial polydactyly, speech impairment, hearing impairment of variable degree and proportionate short stature. This condition represented mild form of Joubert Abstract Genetic Mapping and Mutation Analysis of Genes Causing Human Hereditary Skeletal Disorders XVIII syndrome. Whole exome sequencing in the family revealed a novel in-frame deletion mutation (c.1115-1117delCCT; p.Ser372del) in the MKS1 gene. In silico analysis revealed that Ser372 residue resides in the “B9” interacting region of the MKS1 protein and inframe mutation (p.Ser372del) causes alteration in the conformation of mutant protein with two extra α helixes. The present study described three families (L-N) with split hand/foot malformations. In two families (L, M), genetic mapping followed by Sanger sequencing detected a novel frameshift mutation (c.300-306dupAGGGCGG; p.Leu103Argfs*52) in the WNT10B gene. In the third family (N), whole exome sequencing accompanied by SNP microarray, identified six nucleotides duplication (c.217-222dupCACCCG; p.His73_Pro74dup) in a novel causative gene HOXD8. The work presented in the dissertation resulted in the following publications. 1. Irfanullah, Saadullah Khan, Imran Ullah, C. Arnoud Meijer, Marlies Laurense Bik, Johan T den Dunnen, Claudia AL Ruivenkamp, Marriët JTV Hoffer, Gijs WE Santen, Wasim Ahmad (2016). Hypomorphic MKS1 mutation in a Pakistani family with mild Joubert syndrome and atypical features: expanding the phenotypic spectrum of MKS1-related ciliopathies. American Journal of Medical Genetics Part A 9999A:1–5 2. Irfanullah, Muhammad Umair, Saadullah Khan, Wasim Ahmad (2015). Homozygous Sequence Variants in the NPR2 Gene Underlying Acromesomelic Dysplasia Maroteaux Type (AMDM) in Consanguineous Families. Annals of Human Genetics 79: 238–244 3. Abdul Aziz, Irfanullah, Saadullah khan, Faridullah khan zimri, Noor Muhammad, Sajid Rashid, Wasim Ahmad (2014). Novel homozygous mutations in the WNT10B gene underlying autosomal recessive split hand/foot malformation in three consanguineous families. Gene 534: 265–271. 4. Irfanullah, Abdul Nasir, Sarmad Mahmood, Sohail Ahmed, Muhammad Ikram Ullah, Asmat Ullah, Abdul Aziz, Syed Irfan Raza, Khadim Shah, Saadullah Khan, Muhammad Jawad Hassan, Wasim Ahmad (2016). Identification and in silico analysis of GALNS mutations causing Morquio A syndrome in eight consanguineous families. Turkish Journal of Biology: DOI:10.3906/biy-1607-81 Abstract Genetic Mapping and Mutation Analysis of Genes Causing Human Hereditary Skeletal Disorders XIX 5. Asmat Ullah, Ajab Gul, Muhammad Umair, Irfanullah, Abdul Wali, Farooq Ahmad, Abdul Aziz, Wasim Ahmad (2017). Homozygous sequence variants in the WNT10B gene underlie split hand/foot malformation. Genetics and Molecular Biology (Submitted) 6. Irfanullah, Muhammad Ansar, Saadullah Khan, Abdul Aziz, Wasim Ahmad. Exome sequencing revealed a novel gene KIAA0825 underlying autosomal recessive postaxial polydactyly (In Preparation). 7. Irfanullah, Saadullah Khan, Maaike Verschuren, Marlies Laurense Bik, Johan T den Dunnen, Claudia AL Ruivenkamp, Marriët JTV Hoffer, Gijs WE Santen, Wasim Ahmad. Human HOXD8 is a novel candidate gene causing autosomal recessive split hand foot malformation in a large Pakistani consanguineous family (In Preparation) 8. Irfanullah, Syed Zohaib Tayyed Gilani, Saadullah Khan, Wasim Ahmad. Homozygous mutations in NPR2 gene underlying Acromesomelic dysplasia in Pakistani families (In preparation)