مولانا امتیاز علی خاں عرشی
سخت افسوس ہے گذشتہ ماہ فروری کی۲۵/تاریخ کومولانا امتیاز علی خاں عرشی بھی ۷۷برس کی عمر میں اپنے وطن رامپور میں داعیٔ اجل کولبیک کہہ کراس عالم فانی سے رخصت ہوگئے۔اناﷲ وانا الیہ راجعون۔ مرحوم کی شہرت کاآغاز اوّل اوّل غالبیات کے ماہرکی حیثیت سے ہوا،انھوں نے غالب کے دیوان اور خطوط پرجوتحقیقی مقالات لکھے،انھوں نے اردو زبان وادب کے حلقہ میں دھوم مچادی۔ وہ بیک وقت عربی، فارسی اوراردو تینوں زبانوں اوران کے ادب کے نامور مبصرومحقق تھے۔
وہ رامپور میں۱۹۰۴ء میں پیداہوئے۔رامپور پٹھانوں کی مشہور بستی ہے جو افغانستان کے مختلف قبیلوں سے منسوب ہیں۔ مرحوم کاخاندانی تعلق حاجی خیل قبیلہ سے تھا جویوسف زئی قبیلہ کی ایک شاخ ہے، ابتدائی تعلیم مطلع العلوم نامی ایک مقامی مدرسہ میں پائی۔اسی زمانہ میں پنجاب یونیورسٹی سے عالم کاامتحان پاس کیا۔پھر اورینٹل کالج لاہور میں داخلہ لے کر اولاً مولوی فاضل کااوراس کے بعد منشی فاضل کاامتحان پرئیویٹ طورپر دیا اوردونوں امتحانوں میں درجہ اوّل میں کامیاب ہوئے۔ رامپور واپس آکر مدرسۂ عالیہ کی اونچی کلاس میں داخل ہوئے اور اس سے سند فراغ لی۔تعلیم سے فارغ ہونے کے بعد چند دنوں ندوۃ العلماء کے سفیر رہے، اس سے بیزار ہوکر مستعفی ہوئے توتجارت کرنے لگے، ناتجربہ کاری کے باعث اس میں گھاٹاہوا تو دامن جھاڑ کراس سے بھی الگ ہوگئے۔ آخر۱۹۳۲ء میں رامپور کے مشہور زمانہ کتب خانہ جوتقسیم کے بعد سے رضا اسٹیٹ لائبریری کہلاتا ہے اس سے بحیثیت ناظم کے وابستہ ہوئے۔
کتب خانہ کے ساتھ ان کی یہ وابستگی زندگی کے آخری سانس یعنی کم و بیش نصف صدی تک باقی رہی۔اس مدت میں انھوں نے کتب خانہ کی کیسی عظیم الشان خدمات انجام دی ہیں۔اس کااندازہ اس سے ہوسکتا ہے کہ ملازمت سے سبکدوشی کے عام قانون سے مستثنیٰ کرکے گورنمنٹ نے آرڈر دے دیا ہے کہ...
Background and Aim: The objective of the research is to investigate the impact of lifestyle habits on subjective wellbeing in the presence of role of regulatory emotion self-efficacy as a mediator. Vital for wellbeing, longevity, productivity, relationships, and general quality of life in all areas is a healthy lifestyle.
Methodology: A cross-sectional study has been conducted for 271 Students had been selected as respondents. Smart Pls has been used for calculating the reliability, validity of questionnaire and as well as hypothesis testing.
Results: Food disorder, healthcare anxiety, regulatory emotional self-efficacy have direct and indirect significant impact on subjective well-being. But sleeping disorder has showed the direct and indirect insignificant impact on subjective well-being.
Limitation and Future Implications: Because of time constraints, a lack of comprehension of the research, and a healthy lifestyle people are not aware of health benefits, they had less knowledge about it and were hesitant about a discussion.
Originality: The role of regulatory emotion self-efficacy has not been used as a mediator during the relationship of lifestyle habits and subjective well-being.
Conclusion: Subjective well-being is defined as gratification and satisfaction with one’s life. Regular physical activity is important in order to enhance the self-efficacy and emotional well-being. Good nutrients and a balanced diet provide a person with enough energy to carry out the tasks of daily life effectively.
Intellectually disability is a genetically heterogeneous disorder that results due to impairment in development of nervous system. Intellectual disability is characterized by an IQ level below 70 and limitation in adaptive behaviors. Prevalence of intellectual disability is estimated 2-3% worldwide. In Pakistani population, prevalence of intellectual disability is higher than the average. Numerous factors contribute to the elevated prevalence. These include poor nutrition, deprived social-economic conditions, birth defects, and consanguinity. Genetic factors contributing to intellectual disability have not been studied comprehensively in Pakistani population. The present project was conducted at the Genetic Diseases Laboratory, Center of Excellence in Molecular Biology (CEMB), Lahore. The aim of study was to uncover genetic determinants of intellectual disability in local population. Thirty two families with multiple intellectually disabled patients are enrolled from various cities. Genetic analysis of these families to determine causative genetic variations, homozygosity mapping and next generation sequencing was performed. The results were further verified by in-silico tools and Sanger sequencing. Two families designated PKMR198 and PKMR 216 showed linkage to MRT23 and MRT9 respectively. Two families, PKMR 205 and PKMR 213, showed novel linkage at chromosome 13 and chromosome 1 respectively. Exome sequencing was utilized to find pathogenic DNA changes that have potential to cause intellectual disability. In three families recurrent mutations were found in reported genes for intellectual ability. PKMR29 showed segregation of recurrent mutation c.881A>G in POMT2. PKMR115 presented mutation c.57G>A in SRD5A3. In PKMR184, recurrent mutation c.5769delT was present in SPG11. Novel pathogenic variations were found in ten genes known to be involved in intellectual disability. These pathogenic variations were homozygous in affected individuals. In five families PKMR85, PKMR99, PKMR119, PKMR193 and PKMR133 novel pathogenic missense variations in MED23_c.506A>G, SYNE1_c.939G>C, PGAP1_c.2276A>G, ARL13B_c.599G>A and DOCK8_c.295G>A were segregated with intellectual disability respectively. In another three families PKMR79, PKMR212 and PKMR224 novel disease causing frameshifts variants AP4M1_c.1287delG, ZFYVE26_c.1630_1631delTC and MKKS_c.775delA showed segregation with intellectual disability respectively. One family PKMR102 segregates stop gain variation ASPM_c.3977G>A with microcephaly. A canonical splice site variation AP4S1_c.139-2A>G at splice acceptor site was found segregating with disease phenotype in family PKMR216. In addition, the results revealed pathogenic genetic variations in nine novel candidate genes. In four families PKMR153 PKMR174, PKMR195 and PKMR213 missense damaging variations GPAA1_c.527G>C, MEGF9_c.686G>A, WFDC1_c.634G>A and TMEM222_c.214G>A were segregated with the neurologic impairment. In four families PKMR64, PKMR200, PKMR206 and PKMR215 novel truncating disease causing variations CAPN12_c.658_659delAA, UBE2J2_c.77_78delAA, CCDC82_c.373delG and PUS7_c.89_90delCA showed segregation respectively. In PKMR72 a silent and splice site variation of MDGA2 (c.2232A>G) is segregating. All known and novel pathogenic variations were homozygous in intellectually disable patients and segregate with autosomal recessive inheritance. These findings further expand the existing repertoire of genes involved in ARID.