Wilfred Scawen Blunt and his Ideas on the Future of Islam

Wilfrid Scawen Blunt, like many aristocratic Englishmen in the age of Empire in the late 19th century, took an interest in the Muslim populations of the colonies being governed by Britain. As a prolific writer and poet, his approach differs from his contemporaries in being, on the whole, genuinely sympathetic to Islam. In his book ‘The Future of Islam’ he shows how important the power of Islam in coming centuries is likely to be, and touches upon many important topics, such as the growing spread of Islam in the world and possible adjustments to the Caliphate. He would like to see the formation of a friendly association between Great Britain and the Muslims of the world in the political interests of Britain. Inevitably, many of his predictions and wishes did not materialize in the 20th century. Wilfred Scawen Blunt [1840-1922] was an English gentleman who followed the leisurely pursuits available to affluent members of Victorian society, i.e, travelling and poetry. His travels in the Middle East made a powerful impression on his intellectual and emotional sensibilities. As E.M. Forster wrote in his essay on Blunt, he ‘was drawn to Islam, and at one time thought of professing it.’1 He was, no doubt, in sympathy with the subjugated peoples of the Middle East and with the Indians of South Asia who were groaning under the colonial yoke. Further in the essay, Forster writes, ‘Egyptians found him too proTurkish and Indians too anti-British.’2 This attitude was unique for a stolid Englishman of the time of the ‘highnoon of Empire’. Blunt feared the advance of European powers in Oriental lands. Forster further writes: ‘His detachment is amazing. He dreaded a war because it must involve Asia and Africa, and complete the enslavement of the conservative Oriental nations, whom he loved and who loved him……

Rna Interference Based Therapeutic Interventions for Leukemias

Leukemia, a heterogeneous group of hematological malignancies, continues to cause significant morbidity and mortality despite decades of research and development. Chromosomal aberrations are the main cause of leukemia and lead to the generation of fusion/chimeric genes, resulting in activation of proto-oncogenes and suppression of tumor-suppressor genes. Incidence of different aberrations associated with different leukemias varies in different regions of the world and the data from population based studies in South Asia, including Pakistan, are lacking. The expression of chimeric/fusion genes can be detected using sensitive molecular methods like reverse transcriptase polymerase chain reaction (RT-PCR) and dot blot hybridization. In this study, classic BCR-ABL t(9;22) variants (e13a2 and e14a2) were detected in 96% of CML patients, while one of the patient possessed a unique e13-1a BCR-ABL variant. A total of 68 patients of paediatric ALL, were screened by RT-PCR to determine the relative frequency of t(9;22), t(12;21), t(1;19), and t(4;11,). Translocation (9;22) was seen in 2/68 (3%) and t(1;19) in 2/68 (3) children. Seven children showed t(12;21) while 8 showed t(4;11) translocations. In AML patients, t(8;21) was found in 4/21 patients while t(1;19) was seen in only one of the patient out of 21 screened. Thus, there appears to be a significant under representation of the fusion transcripts for TEL-AML, a good prognostic marker, in this study, unlike in the West, where it is seen in 35% of children with ALL. This, together with the generally increased leukemic burden seen in Pakistani patients, may explain in part, the poor treatment outcome reported. Conventional therapeutic approaches for leukemias include chemotherapy, radiation therapy, interferon therapy, stem-cell transplantation and surgery but their application is limited due to their side effects. The advent of RNA interference (RNAi) technology has opened the door to previously unrefined methods of therapeutic interventions. Gene targeting of the chimeric genes by small interfering RNA is an ideal way to kill tumor cells specifically, while leaving the normal cells unaffected. In case of CML, the over- expressed protein, tyrosine kinase, from BCR-ABL fusion genes, trigger malignant transformation and abnormal proliferation of the cells. Although targeting the BCR-ABL tyrosine kinase activity by imatinib mesylate has rapidly become first-line therapy, drug resistance suggests that combination therapy directed to a complementing target may significantly improve treatment results. To identify such potential targets, we used lentivirus-mediated RNA interference (RNAi) as a tool for functional genomics in human leukemic as well as murine hematopoietic cell lines. Expression of STAT1 and STAT3 proteins was successfully knocked down using specific shRNAs targeting STAT1 and STAT3 mRNA. RNAi-mediated reduction of STAT1 and STAT3 protein expression inhibited BCR-ABL–dependent (K562) but not cytokine-dependent (32D) cell proliferation. The data indicate that BCR-ABL expression may affect the function of normal signaling molecules. Targeting these molecules may harbor significant therapeutic potential for the treatment of patients with CML.