تفسیر القرآن از سر سید احمد خان کا تحقیقی و تنقیدی جائزہ

Sir Syed Aḥmed Khān belonged to a famous family of the subcontinent during the late Mughal and early British colonial period. He was famous for his close relations with the colonial government. He served many years in the judiciary. In recognition of his services, he was conferred upon with various titles such as Sir, The Imperial Advisor, etc. He is the founder of the educational campaign which was later known as the Aligarh movement. He was worried about the future of Muslims in India. This worry forced him to produce various literary and Islamic books to uplift the political, cultural, educational and social status of the Indian Muslims. One of his famous contribution to Islamic literature of Quranic exegeses is his Tafsīr al-Qur’ān. His tafsīr is influenced by western thoughts. He, instead of following the traditional methodology of Quranic exegeses, tried to understand the Quranic verses rationally. This led him to deviate from many established concepts of Islamic doctrines. He went against the Muslims’ affirmed beliefs in his exegesis. He mistrusted some of the basics of Islamic thoughts and tried his best to make new parameters of writing & reading of the Quranic exegesis on human logics. In addition, some of his views show certain relevance to the Mu'tazilites school of thought. The aim of this paper is to present an analytical and a critical evaluation of the exegetical opinions of Sir Syed Aḥmed Khān, particularly on the issues where he deviated from the mainstream Islamic thoughts in his exegesis, Tafsīr al-Qur’ān.

Immunoregulatory Effects of Indoleamine 2, 3-Dioxygenase in Primary Biliary Cirrhosis & Hepatitis C Virus-Induced Liver Cirrhosis

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