69 research outputs found

    An historical study of Isma'il b. 'Abd al-Qadir, "Kitab Sa'adat al-Mustahdi bi-Sirat al-Imam al-Mahdi".

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    Isma'il b. 'Abd al-Qadir (d. I897), a member of a'holy family' of Kordofan, had studied at al-Azhar and later served as mufti in El Obeid, In late 1882 he joined the Mahdi. His subsequent career cannot be fully reconstructed. On 2 Rabi I 1306/6 November 1888, he completed his Sira of the Mahdi, On 6 Shawwal 1306/5 June 1889, he completed another work, dealing with the wars between the Khalifa and the Abyssinians. In 1893, at the Khalifa's order, Isma'il's writings were destroyed and he was banished to al-Rajjaf, where he died in the beginning of 1897. The unique extant manuscript copy of Isma'il's Sira, which forms the basis of the thesis, is a biography of the Mahdi by one of his adherents, which also contains elements of a chronicle. Its history, sources and contents are discussed in the introduction to the thesis. The main historical value of the Sira lies in its presentation of the Turco-Egyptian, the Mahdi and the Khalifa, In addition, it contains many details on ideological, military and other affairs of the Mahdia, and provides an insight into the outlook and frame of mind of an educated Mahdist. The second, and longer part of the thesis is a very full summary, at times approaching a translation, of the text of the Sira. All historically relevant details, including all names of persons, tribes and places, have been retained and, in many cases, annotated. Also, the pagination of the original Arabic manuscript has been indicated. The appendixes include source materials for Isma'il's life (one of them still in manuscript) and a list of proclamations and letters transcribed in the Sira

    A wide-spectrum language for verification of programs on weak memory models

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    Modern processors deploy a variety of weak memory models, which for efficiency reasons may (appear to) execute instructions in an order different to that specified by the program text. The consequences of instruction reordering can be complex and subtle, and can impact on ensuring correctness. Previous work on the semantics of weak memory models has focussed on the behaviour of assembler-level programs. In this paper we utilise that work to extract some general principles underlying instruction reordering, and apply those principles to a wide-spectrum language encompassing abstract data types as well as low-level assembler code. The goal is to support reasoning about implementations of data structures for modern processors with respect to an abstract specification. Specifically, we define an operational semantics, from which we derive some properties of program refinement, and encode the semantics in the rewriting engine Maude as a model-checking tool. The tool is used to validate the semantics against the behaviour of a set of litmus tests (small assembler programs) run on hardware, and also to model check implementations of data structures from the literature against their abstract specifications

    MTADV 5-MER peptide suppresses chronic inflammations as well as autoimmune pathologies and unveils a new potential target-Serum Amyloid A.

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    Despite the existence of potent anti-inflammatory biological drugs e.g., anti-TNF and anti IL-6 receptor antibodies, for treating chronic inflammatory and autoimmune diseases, these are costly and not specific. Cheaper oral available drugs remain an unmet need. Expression of the acute phase protein Serum Amyloid A (SAA) is dependent on release of pro-inflammatory cytokines IL-1, IL-6 and TNF-α during inflammation. Conversely, SAA induces pro-inflammatory cytokine secretion, including Th17, leading to a pathogenic vicious cycle and chronic inflammation. 5- MER peptide (5-MP) MTADV (methionine-threonine-alanine-aspartic acid-valine), also called Amilo-5MER, was originally derived from a sequence of a pro-inflammatory CD44 variant isolated from synovial fluid of a Rheumatoid Arthritis (RA) patient. This human peptide displays an efficient anti-inflammatory effects to ameliorate pathology and clinical symptoms in mouse models of RA, Inflammatory Bowel Disease (IBD) and Multiple Sclerosis (MS). Bioinformatics and qRT-PCR revealed that 5-MP, administrated to encephalomyelytic mice, up-regulates genes contributing to chronic inflammation resistance. Mass spectrometry of proteins that were pulled down from an RA synovial cell extract with biotinylated 5-MP, showed that it binds SAA. 5-MP disrupted SAA assembly, which is correlated with its pro-inflammatory activity. The peptide MTADV (but not scrambled TMVAD) significantly inhibited the release of pro-inflammatory cytokines IL-6 and IL-1β from SAA-activated human fibroblasts, THP-1 monocytes and peripheral blood mononuclear cells. 5-MP suppresses the pro-inflammatory IL-6 release from SAA-activated cells, but not from non-activated cells. 5-MP could not display therapeutic activity in rats, which are SAA deficient, but does inhibit inflammations in animal models of IBD and MS, both are SAA-dependent, as shown by others in SAA knockout mice. In conclusion, 5-MP suppresses chronic inflammation in animal models of RA, IBD and MS, which are SAA-dependent, but not in animal models, which are SAA-independent
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