Formal Specification and Testing of a Management Architecture

The importance of network and distributed systems management to supply and maintain services required by users has led to a demand for management facilities. Open network management is assisted by representing the system resources to be managed as objects, and providing standard services and protocols for interrogating and manipulating these objects. This paper examines the application of formal description techniques to the specification of managed objects by presenting a case study in the specification and testing of a management architecture. We describe a formal specification of a management architecture suitable for scheduling and distributing services across nodes in a distributed system. In addition, we show how formal specifications can be used to generate conformance tests for the management architecture

B-lineage transcription factors and cooperating gene lesions required for leukemia development

Contains fulltext : 118045.pdf (publisher's version ) (Closed access)Differentiation of hematopoietic stem cells into B lymphocytes requires the concerted action of specific transcription factors, such as RUNX1, IKZF1, E2A, EBF1 and PAX5. As key determinants of normal B-cell development, B-lineage transcription factors are frequently deregulated in hematological malignancies, such as B-cell precursor acute lymphoblastic leukemia (BCP-ALL), and affected by either chromosomal translocations, gene deletions or point mutations. However, genetic aberrations in this developmental pathway are generally insufficient to induce BCP-ALL, and often complemented by genetic defects in cytokine receptors and tyrosine kinases (IL-7Ralpha, CRLF2, JAK2 and c-ABL1), transcriptional cofactors (TBL1XR1, CBP and BTG1), as well as the regulatory pathways that mediate cell-cycle control (pRB and INK4A/B). Here we provide a detailed overview of the genetic pathways that interact with these B-lineage specification factors, and describe how mutations affecting these master regulators together with cooperating lesions drive leukemia development