مولانا مفتی حافظ عبداللطیف سہارنپوری
افسوس ہے پچھلے دنوں مولانا مفتی حافظ عبداللطیف ناظم مدرسہ مظاہر العلوم سہارنپور نے چند ماہ کی علالت کے بعد وفات پائی۔جناب مفتی صاحب صاحبِ علم تھے اورصاحب ِباطن بھی۔ فقہ کی جزئیات پربڑی گہری اوروسیع نظر رکھتے تھے۔اخلاق وعادات اورمکارم وشمائل ذاتی کے اعتبار سے سلف صالحین کانمونہ تھے۔ ان کے حسن قابلیت وانتظام کاثبوت اس سے زیادہ اورکیا ہوسکتاہے کہ گزشتہ چند برسوں میں وہ تیز وتند آندھیوں میں بھی مدرسہ کاچراغ جلائے بیٹھے رہے اور اس کوبہرطورقائم وزندہ رکھا،مدرسہ کے ساتھ آں مرحوم کو محبت نہیں، عشق تھا چنانچہ اسی کی خاطر انھوں نے پیرانہ سالی اورضعف ونقاہت کے باوجود پچھلے دنوں برما کاطویل و صبرآزما سفرکیا اوراگرچہ وہاں سے کامیاب وبامراد واپس ہوئے لیکن اپنے ساتھ ایک عارضہ لگالائے اورآخراسی عارضہ میں جان جاں آفریں کوسپردکرکے راہی ملک بقاہوگئے۔رحمہ اﷲ رحمۃ واسعتہً۔
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Background: Controversy occurs in the relationship between serum ferritin levels, insulin resistance and risk of developing anemia in adolescents with family history of diabetes. Aims & Objectives: This study was designed to find out the association between serum ferritin levels with risk of developing anemia in non-diabetic adolescents with family history of type 2 diabetes mellitus (T2DM). Materials & Methods: A descriptive cross-sectional was conducted in a local medical institute of Lahore. Study included 50 non-diabetic, non-obese male / female adolescent with family history of type 2 diabetes mellitus and 50 healthy male/female non-obese adolescents without family history of T2DM considered as controls. Level of serum ferritin and serum insulin was estimated by Enzyme Linked Immunosorbent Assay. Blood glucose was estimated by auto-analyzer. Insulin resistance was calculated by HOMA-IR index and beta cell function was assessed by HOMA- beta index. Results: Levels of fasting blood sugar, insulin resistance were found to be increased with decreased level of serum ferritin and decrease beta cell function in both male as well as female cases as compared to controls. Negative correlation was found between serum ferritin and insulin resistance while a positive correlation was found between serum ferritin and beta cell function. Conclusions: Low level of serum ferritin is associated with reduced beta cell function and increased insulin resistance. This may increase the risk of developing iron deficiency anemia that can affect both immune system as well as increase susceptibility to infections.
Indoleamine 2, 3-dioxygenase (IDO) is an enzyme which is involved in the degradation of L-tryptophan through kynurennine pathway. IDO induced immunosupression can be clinically beneficial for autoimmune diseases. Primary biliary cirrhosis is well defined by autoimmune lesion of intrahepatic bile duct epithelial cells. There is evidence that impaired IDO level contributes to the development of autoimmunity in PBC. Our aim was to assess the expression of IDO in our cell culture model and in PBC patients. Tryptophan metabolites are available and could potentially demonstrate utility in PBC. The current study establishes, for the first time, the expression of IDO in the H69 cell line and increase rate of conversion of tryptophan to kynurenine in patients with PBC. Furthermore, clinical biopsies from PBC patients demonstrated that the expression of IDO was observed not only in cholangiocytes as described earlier but also in hepatocytes. In the presence of TGF-β impaired IDO activity might contribute in the progression of disease scenario. The use of tryptophan metabolites could enhance the effects of IDO and compensate for the lack of efficiency of existing immunotherapeutic strategies. The positive effect of tryptophan metabolites on Human CD4+ T cells to induce polarization toward T-reg phenotype may render a prospective means to ameliorate the consequence of immunotherapy for the management of PBC. In this study we analyzed that the immunomodulatory enzyme IDO activity providing new insight into the pathogenesis of PBC. IDO-mediated immunosupression through tryptophan metabolites may be used against the progression of PBC. Hepatitis C virus (HCV) has infected more than 12 million Pakistani people. Our aim was to assess the expression and enzymatic activity of IDO in HCV patients. We observed high expression of IDO in HCV induced liver cirrhotic patients. IDO was significantly higher in the serum samples of HCV infected patients as compare to the control. It suggest that IDO may involved in the immunosuppression and possibly contribute to progression of HCV infection. Our findings advocated that the HCV patients with over expression of IDO might have poor prognosis, and IDO may become a newly useful marker for HCV induced liver cirrhosis. Thus, blocking IDO might provide new strategies as an adjuvant therapy intervention for HCV. The modeling of the biological regulatory networks (BRNs) using of Rene Thomas Formalism, we observed the critical role of TGF-β and IFN-γ in the suppression and induction of IDO. We observe two types of steady states behaviors in the state graph. The cycle shows the homeostasis of IDO and TGF-β while IFN-γ is inactive (silent). The stable state shows the high expression levels of IFN-γ and IDO while TGF-β is silent. There is a divergence from the cycle towards the stable states and it is observed that this divergence occurs when IFN-γ has expression levels. In cancers condition if we induce TGF-β which is negative regulator of IDO can create the homeostasis. Otherwise the expression of IDO can be inhibited by 1-MT. In case of autoimmune diseases if we inhibit the TGF-β the induction of IDO may produce homeostasis. Tryptophan downstream metabolites can also beneficial in this regard. Key words: IDO, PBC, HCV, IFN-γ, TGF-β, 1-MT, H69, Tryptophan metabolites, BRNs