’’نسیم سخن‘‘ اور صاحبِ کتاب
حافظ محمد اکرم راشدؔ سے میرے دیرینہ اور دیر پا تعلقات ہیں ، یہ ایک علمی خاندان سے تعلق رکھتے ہیں۔ اِن کے بزرگوں کے دینِ اسلام کے میدان میں لگائے ہوئے شجر سایہ دار مسحور کن ماحول پیش کر رہے ہیں اور تشنگانِ علم کی پیاس بجھانے کے لیے دورانِ سفر طلباء کے راستے میں آنے والی جہالت اور کم علمی کی تپش اور دھوپ کو رفع کرنے میں مثالی کردار ادا کر رہے ہیں ۔ میں نے صرف کتاب اور صاحبِ کتاب کے بارے میں چند سطور ضبط تحریر میں لانے کے لیے اپنے قلم کو اذنِ خرام دینا ہے ۔موصوف قلم کے میدان کے شاہسوار ہیں ، ندائے حق کی ادارت ہو، منظور العارفین کی تدوین ہو ، یا منظورالعارفین ٹرسٹ کا قیام ہو، موصوف پیش پیش نظر آتے ہیں ،آپ ہمارے ادارے منظور العارفین ٹرسٹ کے ساتھ قلب و اذہان کی جملہ قویٰ کے ساتھ وابستہ رہے ہیں ۔ مُرور ایّام کے ساتھ پیرانہ سالی اور ضعف کا شکار ہو کر کچھ عرصہ سے گوشہ نشین ہیں تاہم تحریر سے عشق کی حد تک لگائو کی بنا پر کوئی نہ کوئی شاہ پارہ تخلیق کرتے رہتے ہیں ۔ آپ کالم نویس ہونے کے ساتھ ساتھ ایک عظیم خوش نویس بھی ہیں عارفوالااور اس کے مضافات میں خطاطی کے حوالے سے ان کا ایک نام ہے ۔ دنیوی اور دینی تعلیم کے امتزاج کے حامل ہیں اور اپنی ایک شناخت رکھتے ہیں ۔ سرکاری ادارہ میں رئیس مدرسہ کے فرائض سر انجام دے چکے ہیں ۔
مذہبی خدمات کے حوالے سے اِن کی خدمات مہر نیم روز کی طرح واضح ہیں ۔ مرکزی جامع مسجد -N بلاک عارفوالا کی امامت اور خطابت کے فرائض بحسن و خوبی سر انجام دے رہے ہیں۔صاحب ورع اور تقویٰ ہونا اِن کی...
Psychosocial nurturing of children is linked with Parenting and personality development theories and child development theories too report evidences of influences of parenting on children nurturing. The purpose of this paper is to explore existing parenting styles in current literature and how these parenting styles influence upon and form the personality of the children in their early years. The paper aims to examine parenting with reference to authoritarian parenting, authoritative parenting, permissive parenting and uninvolved parenting. It discussed the expectations and responsiveness of the parents which determine their behavior and style. Through parenting, psychosocial nurturing of the children is determined and it was explained in existing literature and analyzed in Islamic teachings. The study followed a critical interpretivist method which examined the literature and conducted content analysis. The study examines the parenting concept and parenting style in Islamic teachings. Islam lays special emphasis on communication and attitude of the parents towards their children particularly in early childhood. Parenting style in Islamic teaching displays a loving and guiding mode. It is less demanding and more responsive in early years. Parenting in Islamic teaching encourages developing tolerance, harmony and peace. It shows flexibility to accept children’s dispositions and tries to discipline their inner faculties. Islamic teachings expect from parents to be responsive with love and passion. It gives children freedom to talk, walk, think and act in a carefree environment where they can become socially and emotionally strong. Parenting in Islam accepts children’s interests and attitudes with positive responses and respects their rights with warmth and love. It particularly develops moral awareness so that children can distinguish between right and wrong and also understand that they need to abide by rules and regulations. Lastly literature also reports that parenting in Islam does not allow any sort of harassment, coercion, frightening and unjust environment for the little angels.
Neurodegenerative movement disorders (NDMDs) is a heterogeneous group of neurological diseases which are caused by selective loss or death of neurons and distinct involvement of functional systems defining movement disability. Proteins with altered physicochemical properties are deposited in the human brain in NDMDs. Not only neurons but glial cells also accumulate these proteins. Intra or extra-cellular Accumulation of structurally deformed and physiologically impotent protein result in the death of neurons as well as glial cells. Neurons are the functional building blocks of the central nervous system, which includes the brain and spinal cord. Mature neurons are post-mitotic and therefore incapable of self-renewal. Morphologically a typical neuron has cell body and processes (Axons and dendrites) which mediate synaptic communication. Glial cells have complex processes extending from their cell bodies; they are generally smaller than neurons. They lack axons and dendrites, do not participate directly in synaptic interactions and electrical signaling, although their supportive functions help define synaptic contacts and maintain the signaling abilities of neurons. NDMDs are incurable and debilitating conditions that result in progressive degeneration and or death of neurons and associated cells. Parkinson‘s disease (PD) is the most common NDMD. Pathologically PD is a complex disease of the mid brain, primarily affecting the substantia nigra (SN) which is densely populated with dopaminergic neurons. The death of SN neurons results in loss of smooth and coordinated skeletal muscle movement. Parkinson‘s disease is generally considered complex and multifactorial disease. Rarely PD runs as a Mendelian trait in families. The familial form of PD is considered to be monogenic. Diverse genetic strategies have been employed to understand genetic risk factors and causes in sporadic and familial forms of PD. Since the genetics of sporadic and familial forms of PD and other NDMDs has not previously been investigated in Pakistan, the objective of this study was to elucidate the role of common genetic risks such as variants in the SNCA, LRRK2, DJ1, CYP2D6 genes in sporadic PD in the Pakistani population and to identify genetic causes of familial PD and other NDMDs in Pakistan. In summary a case-control study, was done and total of 374 subjects including 174 clinically diagnosed PD patients and 200 ethnically matched healthy controls to find Abstract Molecular Genetic Study of Neurodegenerative Movement Disorder in Pakistani Population Page xiv the possible genetic associations and risk factors for Parkinson‘s disease in this population sample. Allele specific PCR and PCR-RFLP was used for screening of previously reported pathogenic single nucleotide polymorphisms (SNPs) in SNCA, LRRK2, DJ1 and CYP2D6 genes. Randomly 20% samples were selected for bidirectional Sanger sequencing to confirm the results. No association was observed for commonly reported variants e.g., rs104893875 (G>A), rs104893877 (G>A), rs104893878(C>G) in the SNCA, rs34805604 (A>G), rs33939927(C>G/T), rs35870237 (T>C), rs34637584 (G>A), rs34778348 (G>A), in the LRRK2 and rs74315354 (G>A) in the DJ1. A strong association was observed in case of rs3892097 (G>A) in the CYP2D6. An increase in the risk of Parkinson by two fold (OR: 2.9; 95% CI 1.5 to 5.50, p = 0.02) was calculated for carriers of rs3892097 (G>A) risk allele (A-allele). Whole genome sequencing and segregation analysis was carried out for three PD families (A, B and C) an atypical Parkinsonian family (D), a Wilson‘s disease family (E) and one family with rare movement disease with periventricular white matter neurodegenerative changes (F). Family (A) with autosomal dominant PD co-segregated with GBA (exon9:c.T1301C:p.434L>P) and PSAP (exon5:c.A470G:p.157N>S) a novel coinheritance of the two genes. Family (B) co-segregated with SEMA6A (exon10:c.G860C:p.287G>A) novel gene (mutation) in autosomal dominant Parkinson‘s disease. Family (C) co-segregated with AAK1 (exon17:c.C2312G p.771P>R) novel gene (mutation) in autosomal recessive Parkinson‘s disease. One family with atypical Parkinson‘s disease Family (D) co-segregated with CSF1R (c.1237G>Ap.G413S) a novel mutation with reported gene for leukodystrophy and atypical Parkinson‘s disease. An autosomal recessive family (E) with Parkinson‘s like symptoms revealed recurrent mutation ATP7B (c.2930C>T p.T977M) for Wilson‘s disease. One family (F) with autosomal recessive movement disorder co-segregated with GPR56 g.57654049 G>C splice site mutation and PCLO exon3:c.G2473A:p.A825T. Minigene assay exclude the splice site mutation in the GPR56 g.57654049 G>C. Thus a novel mutation in PCLO (exon3:c.G2473A:p.A825T) co-segregated in this family.