مسٹر رامانجم
اس وقت دنیا کا سب سے بڑا ریاضی دان ایک ہندوستانی تھا، مسٹر رامانجم کی بابت، جس کے کمالات ریاضیہ کا ذکر آج سے ٹھیک ایک سال قبل معارف میں آچکا ہے، بعض علماء فن کا خیال تھا کہ نیوٹن کے بعد سے دنیا میں اس دماغ کا ریاضی دان نہیں پیدا ہوا ہے اور اس کا تو سب کو اعتراف تھا کہ انھوں نے بعض وہ مسائل حل کردیئے جو پوری ایک صدی سے لاینحل چلے آرہے تھے، سخت افسوس ہے کہ ماہ گذشتہ میں اسی ہستی نے دق میں مبتلا ہوکر دنیا کو اپنے فیض سے ہمیشہ کے لئے محروم کردیا، مرحوم کا سن کل ۳۲ سال کا تھا۔
خوش درخشید ولے دولت مستعجمل بود
(جون ۱۹۲۰ء)
مدراس کے نامور ریاضی دان رامانجم کی خبر وفات کسی پچھلے معارف میں درج ہوچکی ہے، یورپ کے اعلیٰ علمی رسائل مدت تک ان کے ماتم میں سوگوار رہے، اور متعدد ماہرین فن کے قلم نے اس حادثہ عظیم پر علم و فن کی جانب سے فریضۂ تعزیت ادا کیا، کیمبرج یونیورسٹی کے مشہور پروفیسر جی،ایچ، ہارڈی نے سائنٹفک ہفتہ وار نیچر میں جو تعزیت نامہ شائع کیا ہے، اس میں بار بار اس قسم کے فقرہ ملتے ہیں۔ ’’یہ بالکل یقینی ہے کہ مرحوم کی مہندسانہ فضیلت اعلیٰ ترین پایہ کی تھی اور وہ ایک استشنائی قوت فکر و اجتہاد کا شخص تھا‘‘۔ اس کے تقریباً بیس مقالات شائع ہوئے، جنھوں نے زمانۂ جنگ ہی میں تمام دنیائے ریاضیات کو اپنی جانب متوجہ کرلیا‘‘۔ اس کے پیش نظر صرف وہ مسائل تھے، جن تک معدددے چند افراد کی رسائی ہوسکتی ہے‘‘۔ اس کی قوت استنباط بالکل حیرت انگیز تھی، جس کی کوئی نظیر کسی یوروپین ریاضی دان میں...
Ideological Challenges of Atheism to the Muslim Societies and their Solutions from Islamic Perspective It’s a matter of fact that Muslim Societies are facing many socio-political and religious challenges within contemporary dominant waves of thought. One of the serious challenges being faced by the Muslim in the current scenario is Atheism. Although in past era, the Atheism couldn’t become influential with general acceptance of commoners but recently, the ideology of Atheism is spreading fast with statistically reported impact on all religions and civilizations. Atheism is a lack of belief in God, gods or any supernatural being along with the rejection of belief that any deities exist. The philosophy of atheism is nothing new, but it has changed its manifestations over a period. This is obvious that Atheism has now become a serious challenge ideologically and morally for Muslim societies. We are living in a fast-changing society, where preservation of Islamic belief is a challenging task particularly for the new young generation and modern educated lot. Atheists use every possible and available mean and tool for preaching their thoughts and beliefs i.e. Print media, electronic media and above all social media. In this context, this study will explore the questions that; what are the effects of Atheism in Muslim Societies and what is its solution in Islamic perspective? Analytical research methodology will be used in this study. This study perceives that the public and private sector universities are the soft target of Atheism. There is suggested legal, ethical & ideological mechanisms to protect Muslim Societies from threat of Atheism.
Research work, presented in the dissertation, described clinical and molecular analysis of twenty one families (A-U) segregating various types of skeletal deformities. Thirteen of these families (A-M) showed clinical features of dysostosis while eight others (N-U) represent condition of osteochondrodysplasia. After characterizing clinical spectrum in each family, genetic investigation, using various techniques, was conducted to search for the disease genes carrying the responsible sequence variants. Four families (A-D) presented features of split-hand/split-foot malformation (SHFM). Genotyping followed by Sanger sequencing or whole genome sequencing revealed four novel disease causing sequence variants in four different genes including WNT10B, DLX5, DLX6, and TP63. Five families (E-I) showed segregation of polydactyly in autosomal recessive pattern. In two of these families, E and F, whole genome and/or Sanger sequencing revealed two novel sequence variants (p.Arg113*, p.Leu506Glu) in the GLI1. This was the first report of involvement of GLI1 in causing skeletal disorder. In family G, SNPs based genotyping mapped the disease locus at chromosome 4p16.2-4p16.1 and 8q21.3- 8q21.3. However, exome sequencing failed to identify the variant segregating with the disease within the family. In another family (I), a novel locus for Polydactyly was mapped on chromosome 13q13.3–q21.2. Two families J and K presented features of isolated and syndromic form of brachydactyly, respectively. Direct Sanger sequencing revealed a deletion variant (p.Leu176Argfs*17) in the GDF5 in family J and a missense variant (p.Arg921Gln) in the TRPS1 in family K. Variable phenotypes of camptodactyly were found in two families (L and M). Genotyping using microsatellite markers established linkage in both the families at 17p13.3. However, sequence analysis revealed a novel homozygous indel variant (c.252_270delinsGCA; p.Phe85Glufs*108) only in family M. Eight families, presented here, showed various types of osteochondrodysplasia. Three of these families (N-P), segregated Bardet-Biedle Syndrome (BBS) in autosomal recessive pattern. The families N, O and P were mapped to BBS6 (20p12.2), BBS7 (4q27), and BBS8 (14q31.3), respectively. Sequence analysis revealed three novel homozygous mutations including p.Ala96Val in BBS6 in family N, p.Ala194del in BBS7 in family O, and p.Gln449His in TTC8 in family P. Two families Q and R showed frontonasal dysplasia segregating in autosomal recessive manner. SNPs micro-array followed by whole exome and Sanger sequencing revealed two novel disease causing variants including a non-sense (p.Gln202*) in the ALX3 in family Q and splice site (c.661-1G>C) in the ALX1 in family R. Two families, S and T, showed disproportionate short stature segregating in autosomal recessive pattern. Haplotype analysis established linkage of family S to the gene BMPR1B on chromosome 4q22.3. Sanger sequencing revealed a disease causing missense variant (p.Met397Arg) in the BMPR1B in the family. Microsatellite-based genotyping established linkage in the family T on chromosome 16q24.3. Sequence analysis detected a disease causing variant (p.Glu121Argfs*37) in the GALNS gene in family T. In family U, three affected individuals showed Waardenburg anophthalmia syndrome (Anophthalmia-syndactyly). SNPs based homozygosity mapping followed by Sanger sequencing revealed a homozygous missense variant (p.Cys271Tyr) in the SMOC1 gene in the family.