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Home > حضرت ابو ذرٖغفاریؓ کے احوال و آثاراور فضاٗٗئل و مناقب

حضرت ابو ذرٖغفاریؓ کے احوال و آثاراور فضاٗٗئل و مناقب

Thesis Info

Author

محبوب رزاق

Supervisor

علی اصغر چشتی

Institute

Allama Iqbal Open University

Institute Type

Public

City

Islamabad

Country

Pakistan

Thesis Completing Year

2017۔

Thesis Completion Status

Completed

Page

147-ص

Subject

Biography

Language

Urdu

Other

Call No: 922.9742 م ح ح; Publisher: علامہ اقبال اوپن یونیورسٹی،

Added

2021-02-17 19:49:13

Modified

2023-01-06 19:20:37

ARI ID

1676714490367

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صاحبزادہ آفتاب احمد خان

صاحبزادہ آفتاب احمد خان
صاحبزادہ آفتاب احمد خان مرحوم جو مفلوج ہو کر دو سال پہلے سے خاموش ہوچکے تھے، اب وہ ہمیشہ کے لئے خاموش ہوگئے، علی گڑھ کالج نے قومی خدمت گذاروں کی سب سے پہلی جو جماعت پیدا کی تھی، اُس میں صاحبزادہ مرحوم سب سے پیش پیش تھے، وہ سرسید کی پالیسی کے سخت ترین مقلد تھے، وہ مسلمانوں کی سیاسی علمی، تعلیمی، تجارتی، دینی دنیاوی غرض ہر قسم کی ترقی کا ذریعہ جدید تعلیم کو سمجھتے تھے، یہی اُن کا عقیدہ تھا، اسی عقیدہ پر وہ جئے اور اسی پر مرے اُن کے قومی کاموں کاآغاز علی گڑھ کالج اور مسلم ایجوکیشنل کانفرنس سے ہوا، اور اسی پر خاتمہ ہوا، وہ جس مسلک پر تھے، اس پر پوری مضبوطی سے قائم رہے، اُن میں مسلمانوں کی تعلیمی خدمت گذاری کا مخلصانہ ولولہ تھا، اور مسلم یونیورسٹی کی خدمت کا بھی پورا ارادہ رکھتے تھے، مگر افسوس کہ علی گڑھ کی مکدر فضا اُن کی خدمات کو راس نہ آئی، اور یونیورسٹی کو اُن کی کوششوں سے کوئی فیض نہ پہنچ سکا، مرحوم کا دل پسند فلسفہ یہ تھا کہ مسلمان عبدیت اور نیابت الٰہی دونوں کے درمیان تطبیق دیں، یعنی یہ کہ ایک طرف تو وہ خدا کے آگے سرجھکائیں اور اپنے کو اس کا لاچار بندہ سمجھیں، دوسری طرف خدا کی خلافت و نیابت سے سرفراز ہو کر عالم اور کل قوائے عالم پر اپنے علم کے زور سے حکمرانی کریں۔
مرحوم ۴؍ مئی ۱۸۶۷؁ء میں پیدا ہوئے تھے، ۱۸۷۸؁ء میں علی گڑھ کالج میں داخل ہوئے تھے، ۱۸۹۱؁ء میں بیرسٹری کی تعلیم کے لئے ولایت گئے، ۱۸۹۴؁ء میں کامیاب ہوکر واپس آئے، اور علمی گڑھ میں پریکٹس شروع کی، اور ساتھ ہی کالج اور کانفرنس کی خدمت بھی، ۱۹۱۷؁ء میں انڈیا کونسل کے ممبر ہو کر انگلینڈ گئے، اور ۱۹۲۴؁ء...

سیرت طیبہ پر قسِیس زکریا بطرس کی تنقیدات کا تجزیاتی مطالعہ

The Critiques of Zakaria Boutros on the Noble Seerah of the Holy Prophet Muhammad: An Analytical Study Islam is not only a true divine religion but an all-embracing way of life. Prophet Muhammadﷺ is the perfect and ideal role model for the whole mankind. Hisﷺ holy life is open to all in each and every aspect. Hisﷺ noble footsteps and teachings give complete guidance in every walk of life. It has been observed that Jews and Christians’ religious scholars and Orientalist study the Quran, Hadῑth, Islamic History, Culture and Civilization, generally, to deduce negative and subjective conclusions, pretending that they are studying objectively. Father Zakaria Boutros is one such priest from the Middle East. Basically, he is an Egyptian Coptic priest and an active Evangelist. He is a controversial figure in that country for his scriptural studies of Islamic texts. For the last sixty years, he has misguided hundreds of people especially Muslims through his missionary activities and maligning campaign against Islam in the form of booklets, Television programs, Internet services such as Paltalk and personal official websites etc. He has tried to distort facts and to present Prophet Muhammadﷺ in such a way that the attraction of Islam be decreased in the eyes of non-Muslims and doubts be produced among the simple-minded Muslims. In the article under reference, some selected critiques and objections on Prophet Muhammad (ﷺ) related to the birth period (pregnancy duration), lineage, sources of knowledge and accusation of worshipping the black stone, are thoroughly analyzed and responded in a scholarly way.

Clinical and Genetics Charactrization of Human Hereditary Skeletal Deformities in Consanguineous Families

Genetic skeletal disorders (GSDs) constitute a rare, heterogeneous, unique group of bone growth disorders affecting the homeostasis, development of bones, and resulting in anomalous size and shape of the skeleton. Syndromic and non-syndromic skeletal disorders epitomize a public health problem that affects 1/4000 individuals worldwide, thus leading to high health cost and poor quality of life. Detailed information about pathophysiologic mechanisms and disease-causing genetic defects is prerequisite in order to provide proper clinical intervention for different GSDs. With this inkling in mind, the present study was planned to investigate sixteen families manifested with GSDs from different populations at clinical and molecular levels. A total of sixteen families (A-P) segregating different forms of skeletal disorders were genetically and clinically characterized in the present study. The present study was performed in different steps, which included visit to remote areas in Pakistan to construct family pedigree, collection of blood samples, clinical (radiological) examination of at least two affected individuals in each family, genetic linkage analysis using STS microsatellite markers/SNPs microarray, whole exome sequencing (WES) and Sanger sequencing. The identified pathogenic variants were also analyzed for their pathogenicity using in-silico and in-vitro approaches. In the four families (A-D), after failing to establish linkage to the known genes/loci responsible for pre-axial and post axial polydactyly, WES was performed to identify the candidate causing gene. In family A, WES identified a homozygous splice acceptor site variant (c.395-1G>A) in intron 5 of IQCE gene on chromosome 7p22.3. In-vitro analysis using mini-gene splice assay in the family revealed a frameshift variant (p.Gly132Valfs*22). In family B, WES revealed a homozygous missense variant (c.223G>A; p.Asp75Asn) in a potential novel gene GLT8D1 (3p21.1). In family C, a nonsense mutation (c.84C>A: p.Tyr28*) was identified in the C9orf96 (STKLD1) gene mapped on chromosome 9q34.2. The C9orf96 is the first candidate gene identified to cause autosomal recessive non-syndomic pre-axial polydactyly. In family D with autosomal recessive uni-lateral pre-axial polydactyly, WES identified a Abstract XXVI novel biallelic deletion of ZNF468 and ZNF28 genes located on chromosome 19q13.41. In three families, segregating osteogenesis imperfecta, scanning human genome using SNP markers, mapped the causative homozygous region on chromosome 17q21.1- q21.31 in family E and F. Sequence analysis of the previously reported gene FKPB10 on 17q21.1-q21.31 led to the identification of a novel nonsense mutation (c.1490G>A; p. Trp497*) in family E and a previously reported missense variant (c.344G>A; p.Arg115Gln) in family F. In family G, using WES a homozygous splice acceptor site variant (c.359-3C>G) in the intron 2 of the WNT1 gene was identified, located on chromosome 12q13.12. Affected individuals in family H and I were diagnosed with acromesomelic dysplasia type Grebe (AMDG) phenotypes, and those in family J with acromesomelic dysplasia type maroteaux (AMDM). Linkage in families (H and I) was established to the GDF5 locus on chromosome 20q11.22, and in family J to the NPR2 locus on chromosome 9p13-q12. Subsequently, Sanger sequencing of GDF5 gene identified two novel homozygous variants, (c.157_158dupC and c.872G>A) in the family H and I. In family J, an already known homozygous splice donor site variant (c.2986+2T>G) was detected in intron 20 of the NPR2 gene. Three families (K-M), segregating split hand/foot malformation (SHFM) were investigated in the present study as well. Family K and L were subjected to whole genome SNP array analysis. In family K, SNP microarray identified two potential homozygous regions including a 35Mb on chromosome 12 and 11Mb on chromosome 4. This family will be subjected to WES upon availability of funds. Whole genome SNP array following WES in family L revealed a novel frameshift variant (c.409delA; p.Ser137Alafs*19) in the EPS15L1 gene located on chromosome 19p13.11. After establishing linkage in family M to WNT10B on chromosome 12q13.12, Sanger sequencing identified previously reported 7bp duplication (c.300_306dupAGGGCGG) in the WNT10B gene. Clinical and radiological examination of family N and family O showed typical Ellisvan Creveld syndrome (EvC) phenotypes. In family N, WES revealed two homozygous variants in the EVC2 (c.30dupC; p.Thr11Hisfs*45) and TMC1 gene Abstract XXVII (c.1696-1G>A). In family O, WES identified novel compound heterozygous variants (c.919T>C; p.Ser307Pro, c.2894+3A>G) in exon 7 and 20 of the EVC gene. Finally, clinical examination of affected members in family P displayed major features of Bardet-Biedl syndrome (BBS). DNA from an affected individual of the family was subjected to WES. A novel nonsense variant (c.119C>G; p.Ser40*) was identified in exon 1 of MKKS (BBS6) gene located on chromosome 20p12.2. In conclusion, the study, presented here, identified four novel candidate genes, novel and recurrent mutations in few previously reported genes causing different skeletal deformities. The identification of novel skeletal related genes not only improves the overall understanding of skeletal development system but also helps in creating new research dimensions such as understanding different pathways. GSDs results from mutations in different genes that encode different transcription factors (TFs), extracellular matrix proteins, signal transducers (channel proteins, receptors, ligands), RNA processing molecules, tumor suppressors, cellular transporters, enzymes (chaperones), binding proteins, cilia proteins, and numerous proteins having unknown function. The novel gene identified here, such as the IQCE share a common Hedgehog signaling pathway including the EVC/EVC2, thus helping in further understanding there important role in limb patterning, and skeletal developmental. The novel and recurrent mutations might help in the proper genotype–phenotype correlation which will help in prenatal testing and genetic counseling of the affected families. Further functional characterization of the genes, discovered here, is required to elucidate their roles in skeletal development and pathophysiology of myriad skeletal disorders.