382 research outputs found

    An investigation into the deformation and tearing of thin circular plates subjected to impulsive loads

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    Includes bibliographical references.This investigation, primarily experimental, examines the failure of circular plates subjected to impulsive velocities. The experiments are conducted on fully clamped circular steel plates subjected to a uniformly distributed impulse. The strain-rate-sensitive mild steel plates fail with mode I (large ductile deformation), mode II (tensile-tearing and deformation) and mode III (transverse-shear) failure modes. The impulse is measured by means of a ballistic pendulum upon which the test plates are attached. During mode II and mode III failure the complete circumferential tearing of the test plate produces a circular disc. The velocity of this disc is recorded. An energy analysis is performed on the test results and an energy balance equation is formulated. Einput = Edeformation + Etearing + Edisc. The input and disc energies are obtained from the experimental measurements and the deformation energy is predicted by using the final deformed height and a shape function together with a rigid-plastic energy analysis adopted by Duffey. Etearing refers to the energy for tensile-tearing in mode II failure or the energy for transverse-shear in mode III failure. Good correlation is found and the experiments show good repeatability. The threshold velocities for the onset of failure modes II and III are given

    A study on the response of single and double circular plates subjected to localised blast loading

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    The response of single and double layered steel plates to localised air-blast loading was examined. Two configurations, both comprising fully clamped circular plates with a 200 mm exposed diameter, were considered: 4mm thick single and (2+2) mm double layered plates. The localised air-blast loading was applied by centrally detonating discs of PE4 plastic explosive. Similar failure modes were evident in the single and double plate configurations, namely, Mode I (large inelastic deformation) and Mode II (capping failure along with deformation) responses. The double plates exhibited larger midpoint deflections than the single plates, and partial tearing of the front plate in the double plates was observed at a lower impulse than in the single plates. However, complete capping of both plates in the double plate configuration occurred at the same charge mass as for the single plates, implying that both configurations offer equivalent protection from capping failure as a result of this type of localised blast loading. A metallographic study of the deformed and torn plate regions did not reveal any phase transformation in the steel. It was also found that the 2 mm thick plates exhibited larger increases in grain size than the 4 mm thick plates

    Antibodies Against Human BLyS and APRIL Attenuate EAE Development in Marmoset Monkeys

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    B lymphocyte stimulator (BLyS, also indicated as BAFF (B-cell activating factor) and CD257), and A Proliferation Inducing Ligand (APRIL, CD256) are two members of the TNF superfamily with a central role in B cell survival. Antibodies against these factors have potential therapeutic relevance in autoimmune inflammatory disorders with a proven pathogenic contribution of B cells, such as multiple sclerosis (MS). In the current study we performed a multi-parameter efficacy comparison of monoclonal antibodies against human anti-BLyS and anti-APRIL in a common marmoset (Callithrix jacchus) model of experimental autoimmune encephalomyelitis (EAE). A MS-like disease was induced by immunization with recombinant human myelin/oligodendrocyte glycoprotein (rhMOG) in complete Freund's adjuvant. The results show that the anti-BLyS and anti-APRIL antibody cause significant depletion of circulating CD20+ B cells, but a small subset of CD20 + CD40highB cells was not depleted. Induction of CD20+ B cell depletion from lymph nodes was only observed in the anti-BLyS treated monkeys. Both antibodies had a significant inhibitory effect on disease development, but all monkeys developed clinically evident EAE. Anti-BLyS treated monkeys were sacrificed with the same clinical signs as saline-treated monkeys, but nevertheless displayed significantly reduced spinal cord demyelination. This effect was not observed in the anti-APRIL treated monkeys. The two antibodies had a different effect on T cell subset activation and the profiles of ex vivo released cytokines. In conclusion, treatment with anti-BLyS and anti-APRIL delays the development of neurological disease in a relevant preclinical model of MS. The two mAbs achieve this effect via different mechanisms

    Identification of dimethylamine monooxygenase in marine bacteria reveals a metabolic bottleneck in the methylated amine degradation pathway

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    Methylated amines (MAs) are ubiquitous in the marine environment and their subsequent flux into the atmosphere can result in the formation of aerosols and ultimately cloud condensation nuclei. Therefore, these compounds have a potentially important role in climate regulation. Using Ruegeria pomeroyi as a model, we identified the genes encoding dimethylamine (DMA) monooxygenase (dmmABC) and demonstrate that this enzyme degrades DMA to monomethylamine (MMA). Although only dmmABC are required for enzyme activity in recombinant Escherichia coli, we found that an additional gene, dmmD, was required for the growth of R. pomeroyi on MAs. The dmmDABC genes are absent from the genomes of multiple marine bacteria, including all representatives of the cosmopolitan SAR11 clade. Consequently, the abundance of dmmDABC in marine metagenomes was substantially lower than the genes required for other metabolic steps of the MA degradation pathway. Thus, there is a genetic and potential metabolic bottleneck in the marine MA degradation pathway. Our data provide an explanation for the observation that DMA-derived secondary organic aerosols (SOAs) are among the most abundant SOAs detected in fine marine particles over the North and Tropical Atlantic Ocean
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