حکیم عبد النبی شجرطہرانی(۱۹۶۸۔۱۸۷۲) ہمیر پور جموں میں پیدا ہوئے۔ اصل نام عبد النبی اور شجر تخلص کرتے تھے۔ آپ کے والد دہلی میں طبیب تھے۔۱۹۰۲ء میں آپ نے میڈیکل کالج لکھنؤ سے طب کی سند حاصل کی۔(۶۲) ۱۹۲۰ء میں آپ نے والدین سمیت جموں سے ہجرت کی اور سیالکوٹ میں مستقل سکونت اختیار کی۔ (۶۳) جب شجر میڈیکل کالج لکھنؤ میں طالب علم تھے تو اسی دور میں آپ کو حضرت داغ دہلوی سے تلمذ ہوا۔ اس دور میں شجر اپنا کلام داغ دہلوی کو دکھایا کرتے تھے۔(۶۴) شجر سند یافتہ طبیب تھے۔ آپ فوجی ڈاکٹر کی حیثیت سے برطانوی فوج میں شامل ہوئے۔ مولانا جوہر اور مولانا شوکت علی کے ساتھ تحریکِ خلافت کے دوران متعدد جلسوں میں حصہ لیا۔۱۹۲۰ء میں آپ نے کانگریس کی رکنیت اختیار کی۔ بعد ازاں کانگریس چھوڑ کر مجلسِ احرار میں شامل ہو گئے۔(۶۵) شجر کے عطاء اﷲ شاہ بخاری سے گہرے مراسم تھے جب وہ سیالکوٹ آتے تو شجر کی قیام گاہ پر قیام کرتے۔ شجر نے ۸۰ سال متحرک ادبی زندگی گزاری اور تقریباً ایک لاکھ شعر کہے۔ ان کی باقیات کے پاس ان کے بائیس شعری مسودات محفوظ ہیں لیکن ان کے اکثر مسودے نایاب ہیں اور گم ہو گئے ہیں۔(۶۶) شجر کی زندگی میں ان کا پہلا شعری مجموعہ ’’صبرِ جمیل‘‘ ۱۸ اگست ۱۹۲۸ء کو شائع ہوا۔ اس کا مکمل نام مثنوی سرگزشت یتیم المعروف صبرِ جمیل ہے۔ شجر نے اس میں ایک یتیم کی سرگزشت کو اپنے اشعار میں پیش کیا ہے۔ اس میں صبر‘ استقلال و صداقت‘ تقویٰ و ذہانت‘ عصمت دنیاوی‘ انقلابات اور عروج و زوال جیسے مضامین نہایت خوبی سے نبھائے گئے ہیں۔ دوسراشعری مجموعہ ’’زبانِ فطرت‘‘ جو نظموں پر مشتمل ہے، ۱۹۲۹ء کو مقبول عام پریس لاہور سے منشی غلام احمد نے شائع کیا۔ اس مجموعے میں خارو گل‘ نسیم و بہار‘ شام و سحر‘ روز و شب اور نورو ظلمات کے تعلق...
Allama Usaid-ul-Haq Badayuni (1975-2014) was a great Islamic thinker, researcher and religious scholar. He wrote 14 Islamic books were on academic and research works. 17 books were arranged and prefaced by him. 12 books were translated and reviewed by him. 22 books were completed under his supervision. The book “Quran ki Saainsi Tafseer” (Scientific exegesis of Quran) authored by Allama Usaid-ul-Haq Qadri Badayuni is an educational, scholarly and critically acclaimed masterpiece. A comprehensive explanation and meaning of scientific exegesis are given at the beginning of this book. After that, the opinions of the modem and contemporary scholars regarding the justification and non-justification of the scientific interpretation are presented lucidly. The differences between the Quran and Science and several misinterpretations of the scientific exegesis have also been recorded. The conditions set by Islamic scholars and researchers regarding the justification of scientific exegesis have been explained in the book. This book of Allama Badayuni is a wonderful addition to the chapter of scientific exegesis in terms of research and critics. And this book will be remembered as an academic reference in the history of Indo-Pak. KEYWORDS
Cardiovascular disease (CVD) contributes to high morbidity and mortality rates around the world. Coronary artery disease (CAD), hypertrophic cardiomyopathy (HCM), and idiopathic dilated cardiomyopathy (IDCM) are among CVD phenotypes which are affected by genetic and environmental factors. In addition to primary risk factors, single nucleotide polymorphisms (SNPs) in inflammatory cytokines like resistin gene (RETN) and tumor necrosis factor-alpha (TNF-alpha) are considered to influence the pathogenesis of CVD. Resistin is a relatively novel inflammatory marker, whereas TNF-alpha gene polymorphism has been widely investigated in patients with CVD among different ethnic populations with conflicting results. In the present study the RETN SNPs at -420 C>G (rs1862513) and +299 G>A (rs3745367), and the TNF-alpha gene SNPs at -308 G>A (rs1800629) and +238 G>A (rs361525) were investigated to determine the association of the cytokines’ mutant genotypes with the pathogenesis of CAD, HCM and IDCM in a Pakistani population. Blood samples were obtained from families (n = 40 families) with CAD history, sporadic CVD cases (n = 718), and healthy control subjects (n = 720) randomly selected from the regions of CVD cases. Biochemical analysis of lipids and high sensitivity C-reactive protein (hs-CRP) was carried out spectrophotometrically, while serum resistin levels were determined by enzyme-linked immunosorbent assay (ELISA). RETN and TNF-alpha genotyping was performed by polymerase chain reaction (PCR) and DNA sequencing or restriction fragment length polymorphism (RFLP). The evaluation of the RETN -420 C>G and +299 G>A polymorphism in a case- control study from forty complex Pakistani families with CAD history revealed that the said SNPs were significantly associated with the pathophysiology of CAD (P < 0.0001 for both SNPs). Heritability of the susceptible/variant alleles was investigated from parent–offspring trios in these families by using the transmission disequilibrium test (TDT) analysis. Data showed preferential transmission of the disease susceptible alleles from parent to affected off-spring (P < 0.0001 for both SNPs). Elevated resistin and hs-CRP levels were observed from familial CAD cases vs. unaffected subjects of the families (P < 0.0001 for both markers). The present study revealed that the RETN−420 C>G and +299 G>A variant genotypes were significantly associated with Resistin and Tumor Necrosis Factor-Alpha Gene Polymorphism and the Risk for Cardiovascular Disease in a Pakistani Population high concentrations of lipid biomarkers, resistin, and hs-CRP in familial cases of CAD (P < 0.05 for each variable). The TNF gene polymorphism at -308 and -238 was investigated in sporadic CAD cases, and healthy subjects of the study population. The findings demonstrated a significant link between the TNF-308A variant allele and CAD, whereas the -238 SNP was not associated with the disease. Further, RETN SNP at -420 was investigated in patients with HCM. The results demonstrated an association between the RETN -420 C>G polymorphism and cardiac hypertrophy in the study population (P < 0.0001). Logistic regression analysis revealed a significant association of the serum resistin levels (P < 0.0001) and the RETN -420 C>G polymorphism (P = 0.001) with the disease. Data from this investigation was published as a pioneer report on the association of the RETN -420 C>G polymorphism with HCM. The current study also demonstrated a link between the RETN -420 C>G (P < 0.0001) and +299 G>A (P = 0.0007) polymorphism and IDCM cases vs. healthy controls of the study population. The RETN -420G and +299A haplotype was more prevalent in the patient vs. control group (P < 0.0001). The results suggest that the RETN -420 C>G and +299 G>A polymorphism may have a role in the pathogenesis of IDCM. The current research leads to conclusion that the RETN SNPs at -420 and +299 are associated with familial cases of CAD in Pakistani families with the disease history. It was observed that the disease-susceptible alleles from parents to affected off-springs were transmitted more frequently in a family trios study. Regarding the TNF-alpha, it was observed that the -308 SNP was associated with the pathogenesis of CAD in the study population, whereas the variant genotype at -238 showed no link with the disease. Furthermore, this study demonstrated that the RETN -420 C>G polymorphism is associated with HCM in the study population; this was a pioneer finding in relation to the disease. Another interesting data from this study revealed that the RETN -420 C>G and +299 G>A polymorphism is associated with pathology of IDCM in the study population; the said SNPs have not been investigated among other populations prior to this study. This study concludes that the RETN and TNF- alpha gene polymorphisms are significantly associated with the pathogenesis of CAD and cardiomyopathy in the study population. Resistin and Tumor Necrosis Factor-Alpha Gene Polymorphism and the Risk for Cardiovascular Disease in a Pakistani Population XVII Abstract Some data from the present study has been published in the following papers: Hussain S, Bibi S, Javed Q (2011). Heritability of genetic variants of resistin gene in patients with coronary artery disease: a family-based study. Clinical Biochemistry 44: 618-622. Hussain S, Asghar M, Javed Q (2010). Resistin gene promoter region polymorphism and the risk of hypertrophic cardiomyopathy in patients. Translational Research 155: 142-147.