یوسف نیر(۱۹۴۷ء ۔۲۰۱۷) کا اصل نا م یوسف رحمت ہے اور نیر تخلص ہے ۔ آپ محلہ اٹاری گیٹ سیالکوٹ میں پیدا ہوئے۔(۱۰۹۰) آپ نے ایم ۔اے اردو پنجاب یونیورسٹی اور ایم۔فل اردو علامہ اقبال اوپن یونیورسٹی سے کیا۔ ۱۹۷۹ء میں آپ کی تعیناتی بطور لیکچرار گورنمنٹ کالج رحیم یار خان میں ہوئی۔ گورنمنٹ کالج سیالکوٹ سے ایسوسی ایٹ پروفیسر کے عہدے پر آپ ریٹائر ہوئے ۔(۱۰۹۱) آپ کالج میگزین lکے مدیر رہے اور ان کی ادبی تخلیقات اس میں شائع ہوتی تھیں۔ آپ کا شعری کلام ’’کاتھولک‘‘،’’نقیب‘‘ ،لاہور ،’’شاداب ‘‘ لاہور ، ’’شعاعِ نور‘‘ ،لاہور ،’’بیسویں صدی‘‘ ،لاہور اور ’’فنون ‘‘ لاہور میں شائع ہوتا رہا۔
آپ مرے کالج کی مجلسِ سخن اور مجلسِ اقبال کے انچارج رہے۔ نیرمرے کالج کے علمی و ادبی مجلہ ’’الفیض ‘‘ کے نگران رہے اور مرے کالج سے اقبال نمبر اور غالب نمبر شائع کیے۔۱۹۸۸ء میں آپ پاکستان رائٹرز گلڈ کے مرکزی صدر منتخب ہوئے۔ پنجابی ادب سنگت لندن نے انھیں ۲۰۰۰ء کاادبی ایوارڈ لندن میں ایک مشاعر ے میں پیش کیا۔ (۱۰۹۲)’’روشنی کا پہلا دن‘‘ یوسف نیر کا شعری مجموعہ الحمد پبلی کیشنز نے ۱۹۹۲ء کو شائع کیا۔
یوسف نیر ادب میں ادب برائے زندگی نظریے کے قائل ہیں۔ انھوں نے اپنی شاعری میں ہمیشہ غریب ،مظلوم اور پسماندہ معاشرے کے پسے ہوئے انسانوں کے دکھ اور محرومی کی بات کی ہے۔ وہ ظالم ،جابر اور استحصالی نظام اور افراد کی مـذمت کرتے ہیں۔ نیر گہرا سماجی شعور رکھتے ہیں وہ سماجی اور معاشرتی ظلم و ستم کو نظر انداز نہیں کرتے بلکہ اسے محسوس کرتے ہیں اور اپنی شاعری میں جا بجا بیان کرتے نظر آتے ہیں:
راہ کوئی نہیں ہے بچنے کی……
1ہر طرف شیش ناگ بیٹھے ہیں
During the former era of the State of Bahawalpur the Nawabs were in perpetual conflict with their relatives. The Kehlwar family of Sindh and during the modern era remained under influence of the British. So we can say that the State of Bahawalpur remained under constant foreign influence and the Nawabs did not have chance to rule with liberty and ease. In spite of these facts, the government of the State had many Islamic qualities and there are clear effects of Fatwa on judicial system in both eras.
β thalassemia is the most prevalent autosomal recessive disorder characterized by absence or reduced production of hemoglobin (Hb) levels, primarily caused by mutations on β globin locus. β thalassemia is heterogeneous at the molecular level, presenting variable phenotypes accompanied with severe medical complications. Current standard of care for clinical management of β thalassemia includes regular, long-life safe blood transfusion along with appropriate iron chelation therapy. At present, the only permanent cure is bone marrow transplantation. An emerging and exciting therapeutic approach to handle β thalassaemia is production of fetal hemoglobin (HbF) which is major Hb of fetal life. In recent years, Hydroxyurea (HU) has proven to be a promising HbF augmenting agent but response to HU therapy varies from transfusion elimination to insignificant clinical response. Various approaches are being made to understand the mechanism HbF augmentation with differential responses. Advancement in proteomics offers an efficient tool to study differential proteome in response to treatment leading towards precision and personalized medicine. This study is designed to improve mechanistic understanding of proteomic changes that HU therapy exerted on β thalassemia patients, in consort with deciphering differential protein expression in HU responder and non-responder. Firstly, samples were subjected to twodimensional gel electrophoresis to assess differentially expressed proteins. Later, differential proteins were identified by label free quantitative proteomics approach. Two hundred and eighty seven proteins were identified with two or more unique peptides in samples studied. Among these, twenty eight proteins were found to be significantly different in pre versus post HU treated β thalassemia patients at probability of < 0.05. Eighteen proteins were down-regulated while ten were found to be up-regulated after HU treatment. Clinically important proteins include Hemopexin (HPX), Haptoglobin (HP), Haptoglobin-related protein (HPR), Hemoglobin subunit beta (HBB), Hemoglobin subunit delta (HBD), Hemoglobin subunit alpha (HBA1), Protein S100-A8 (S100A8), Apolipoprotein L1 (APOL1), Apolipoprotein C-I (APOC1), Transferrin receptor protein (TFRC), Complement C4-A (C4A), Apolipoprotein A (LPA), Ceruloplasmin (CP) and Ficolin-3 (FCN3). HU therapy in β thalassemia patients started reverting protein profile towards healthy pattern, in addition with decrease in transfusion requirements. A follow up study on plasma of HU treated β thalassemia patients was performed to compare proteomic profile of HU responder and non-responder. Twenty six proteins were found to be differentially expressed in HU responder versus non-responder at p < 0.05. Among these, fifteen proteins showed a significantly increased level while eleven proteins revealed a decreased in expression. Clinically relevant altered proteins in HU responder are Peroxiredoxin-2 (PRDX2), Carbonic anhydrase 1(CA1), Hemoglobin subunit gamma-1 (HBG1),Hemoglobin subunit beta (HBB), Hemoglobin subunit delta (HBD), Hemoglobin subunit alpha (HBA1), Properdin (CFP), Cholinesterase (BCHE), Phospholipid transfer protein (PLTP) and Plasma protease C1 inhibitor (SERPING1). We suggest that further research would be required for validation of identified proteins in large cohort to endorse as potential predictive biomarker for HU therapy. Considering the association of oxidative stress with β thalassemia, we also studied markers of oxidative stress in response to HU therapy in β thalassemia covering Paraoxonase1 (PON1), Reactive oxygen species (ROS), and Malondialdehyde (MDA). Although PON1 serve as an antioxidant to reduce the adverse effects of the oxidative stress in β thalassemia, our results indicate that mode of action of HU may not directly be through oxidative imbalance