Aircraft control mechanisms, such as those that operate the flaps, ailerons, rudders, etc., are almost exclusively driven by hydraulic-based systems. Their popularity in flight control systems is not unfounded; hydraulic actuators are quite torque-dense and benefit from decades of development bringing operating performance to a high level. On the other hand the infrastructure to support this system increases weight, adds system development complexity, and reduces aircraft maintainability [Jensen et al, 2000]. Based on recent Electro-Mechanical Actuator (EMA) development and design efforts at the Robotics Research Group (RRG), a new opportunity exists to replace current hydraulic flight control systems with those powered by electricity through a national program [Tesar, 2005]. A literature review of the topic found a 30 year old effort by AiResearch to develop a similarly powered hingeline actuator with given traditional performance goals (torque capacity, redundancy, output speed, reliability). In this report,a thorough analysis is performed on each major component group to quantitatively evaluate this baseline device. Using component technologies developed at RRG, this report proposes a dual torque-summing electromechanical actuator, each with a star compound / hypocyclic combined gear train, designed to exceed the performance of the original (1976) AiResearch project. This preliminary design exercise includes a layout of the entire actuator along with an appropriate analysis of major components including bearings, gear train, motor, housing, and release mechanism. The performance of this gear train is critical to overall actuator success and fundamental analytics have already been developed in this area [Park and Tesar, 2005]. Finite Element Analysis on the gear train and housing provide early design feedback and verification of actuator performance characteristics. In particular, simulation results show the gear stiffness, load sharing, and torque capacities exceed analytical estimates. Finally, four different comparisons are presented that evaluate configuration variations of the two designs based on applicable performance criteria. Results show the RRG fault-tolerant actuator has a marked improvement over the baseline in average stiffness (14.2x), reflected inertia (3.2x) and nominal torque density (3.4x). The chapter next lists actuator test methods and aircraft qualification standards. Finally, a summary of future work is detailed in a ten step outline to bring this EMA technology to a level of early deployment in a large range of aircraft systems.

Mode of access: World Wide Web. / Thesis (Ph. D.)--University of Hawaii at Manoa, 2005. / Includes bibliographical references (leaves 116-154). / Electronic reproduction. / Also available by subscription via World Wide Web / xvii, 157 leaves, bound ill. 29 cm

Thesis (Ph. D. in Cancer Biology)--Vanderbilt University, May 2008. / Title from title screen. Includes bibliographical references.

Thesis (Ph. D.)--Michigan State University. Dept. of Chemistry, 2007. / Title from PDF t.p. (viewed on Apr. 16, 2009) Includes bibliographical references. Also issued in print.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 1993. / Vita. Abstract. Includes bibliographical references (leaves 154-169). Also available via the Internet.

Thesis (Ph. D.)--McMaster University, 2003. / Advisor: Michael Rudnicki. Includes bibliographical references (leaves 187-228). Also available via World Wide Web.

Slits and their Roundabout (Robo) receptors were identified based on their role in regulating axon guidance, but are known to play multiple roles in development, including regulating heart development and myoblast migration. There are 3 vertebrate Slits (Slit1 – 3) and 4 Robos (Robo1 – 4), and previous work has demonstrated expression of Slit and Robo family members in and around developing joints where their function is unclear. Mutations in human Robo3 have been linked to degenerative joint disorders, such as scoliosis and rheumatoid arthritis. Misregulation of other members of the Slit/Robo signalling pathway is also reported in cells from arthritic joints. This suggests that Slit/Robo signalling is required for normal joint development and/or maintenance, though our understanding of their roles in these processes is rudimentary. The central question of my thesis is to determine the role/s of Slit/Robo signalling in limb and joint development. In situ hybridisation confirmed strong expression of Slits and Robos throughout mouse limb and joint development, though no expression of Slit1 or Robo3 was detected. Analysis of Slit1/2, Slit3 and Robo1 mutant (loss-of-function) mice revealed normal limb development, however misexpression of dominant-negative Robo2 during chicken limb development caused shortening of cartilage elements. To begin to identify molecular changes that may compensate for the loss of Slit/Robo signalling I demonstrated members of the Sema3/PlexinA/Nrp axon guidance family are expressed in patterns comparable to those of Robo1, Robo2 and Slit3. I discovered that PlexinA1 is downregulated in Slit3 mutant mouse limbs. My results suggest the role for Silt/Robo signalling may be more complex than previously thought and do not define a clear role for signalling during limb development. My results suggest the role for Silt/Robo signalling may be more complex than previously thought and do not define a clear role for signalling during limb development. Previous work has linked Slit/Robo signalling to development of degenerative joint disorders, and I propose some hypotheses as to how Slit/Robo signalling could cause bone and joint defects.

Amino acid deprivation of Escherichia coli results in the accumulation of guanosine 5'-triphosphate 3'-diphosphate and guanosine 3', 5'-bispyrophosphate, collectively designated (p)ppGpp. These nucleotides are synthesized by a ribosome-associated enzyme encoded by the relA gene and are thought to represent starvation stress signal molecules. They may mediate the global reorganization of cellular metabolism, known as the stringent response, that is characteristic of starving bacteria and which apparently represents a survival strategy. In this dissertation, the following aspects of the stringent response are characterized: (i) the temperature phenotypes of relA mutants; (ii) the C-terminal domain of RelA; and (iii) the role of RelC (ribosomal protein L11) in the regulation of RelA. All three of the commonly used relA mutant alleles of E. coli, relA1, relA2, and ∆relA251::kan, conferred temperature-sensitive (ts) phenotypes. The temperature sensitivity was associated with decreased thermotolerance, and relA mutants were killed at temperatures as low as 42°C. The ts phenotypes were suppressed by increasing the osmolarity of growth media and by certain mutant alleles of rpoB, the gene encoding the β-subunit of RNA polymerase, suggesting a defect in transcription. DNA in heat-shocked wild type bacteria was initially relaxed but the normal level of negative supercoiling was restored within 10 min after heat shock. In contrast, DNA in heat-shocked relA mutants remained relaxed. This relA-associated defect in DNA negative supercoiling was suppressed by increased medium osmolarity. Furthermore, the re/A-mediated ts phenotype was suppressed by low concentrations of novobiocin, a specific inhibitor of the B subunit of DNA gyrase. Moreover, low concentrations of novobiocin restored DNA negative supercoiling in the relA mutant at high temperature. Based on previous reports, it is proposed that low concentrations of novobiocin induce the synthesis of the DNA gyrase A and B subunits, and the resulting increase in DNA gyrase activity restores normal supercoiling at high temperature. Collectively, the data suggest that relA mutants are unable to efficiently transcribe key genes required for thermotolerance, and this defect is related to their inability to restore negative supercoiling of DNA at higher temperatures. In addition, the proposed defect in transcription may be related to the observation that ppGpp binds to the p-subunit of RNA polymerase. The portion of relA encoding the C-terminal half of RelA (starting at amino acid 455), designated 'RelA, was subcloned. Overexpression of 'RelA relaxed the stringent response by inhibiting (p)ppGpp synthesis during amino acid deprivation. 'RelA represented the ribosome-binding domain, and when overexpressed, 'RelA somehow replaced RelA on ribosomes. The 'RelA ribosome-binding domain was further localized to a region between amino acids 455 to 682 with the main binding activity in a fragment extending from amino acids 560 to 682. Several criteria were used to establish the fact that 'RelA also mediated the formation of homodimers. These included co-purification of RelA and 'RelA, glutaraldehyde protein crosslinking, and analysis by nondenaturing polyacrylamide gel electrophoresis. The dimerization domain overlapped with the ribosome-binding domain. Affinity blotting assays using 'RelA as a probe revealed RelA and 'RelA as the only proteins in crude cell extracts that bound 'RelA. Therefore, these studies failed to identify the ribosomal components that interact with RelA. Amino add-deprived rplK (previously known as relC) mutants of E. coli cannot activate ribosome-bound RelA and consequently exhibit relaxed phenotypes. The rplK gene encodes ribosomal protein L11, suggesting that L11 is involved in regulating the activity of RelA. The overexpression of derivatives of rplK that contained short N-terminal deletions that eliminated the proline-rich helix resulted in relaxed phenotypes. In contrast, bacteria overexpressing normal L11 exhibited a typical stringent response. The L11 mutant proteins were incorporated into ribosomes. A derivative in which Pro22 was changed to Leu22 was constructed by site-directed mutagenesis. This amino add substitution was sufficient to confer a relaxed phenotype when it was overexpressed. A variety of methods were used in attempts to demonstrate a direct interaction between L11 and RelA, but all yielded negative results. These results indicate that the N-terminal proline-rich helix, and Pro22 in particular, is directly involved in activating RelA activity during amino acid deprivation. The mechanism apparently does not involve a direct interaction between RelA and L11 and is presumably mediated by another ribosomal component. / Graduate

This paper gives an overview of workflow management systems (WfMSs) and their security requirements with focus on access mechanisms. It is a descriptive paper in which we examine the state of the art of workflow systems, describe what security risks affect WfMSs in particular, and how these can be diminiuished. WfMSs manage, illustrate and support business processes. They contribute to the performance, automation and optimization of processes, which is important in the global economy today. The security of process flows is important, since the sensitive business data need to be protected to inhibit illegal activities, such as blackmailing, imitation and fraud and to provide for good customer service. This paper focuses on access mechanisms, because they are basic security mechanisms used by WfMSs assuring that only authorized users are provided access to data and resources. Also because of the unsecurity of the Internet, which is commonly used as infrastructure of Workflow systems, additional security mechanisms, such as PKIs, digital signatures and SSL have to be used to provide secure workflows. Depending on the particular requirements in workflow systems, different extensional access control (AC) mechanisms have been developed to maintain security. But when it comes to commercially used WfMSs, the availability of the system is of utmost importance. It is the prerequisite for the system to be employed by companies. The problem is that there is always a trade-off between availability of the system and security. Because this trade off is generally solved in favor of availability, a major part of the developed AC mechanisms are not used in commercially used WfMS. After the first part of this paper which is rather theoretical, we examine a commercial WfMS, namely IBM's MQ Workflow , and its security mechanisms. We show vulnerabilities of the system that could be abused by attackers. Afterwards, we show which security mechanisms, in particular, AC mechanisms are provided to secure against threats. We conclude with a summary, which highlights the difference between security concepts developed in the research area and those really implemented by the commercially used WfMS.

The cellular regulation of acidification and intracellular ph (pHi) was studied in the integument of Rana pipiens, a model renal epithelium. Acidification was enhanced by : (1) chronic metabolic acidosis, (2) high salinity adaptation, and (3) ibuprofen treatment.