8,559 research outputs found

    Postbuckling behavior of graphite-epoxy panels

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    Structurally efficient fuselage panels are often designed to allow buckling to occur at applied loads below ultimate. Interest in applying graphite-epoxy materials to fuselage primary structure led to several studies of the post-buckling behavior of graphite-epoxy structural components. Studies of the postbuckling behavior of flat and curved, unstiffened and stiffened graphite-epoxy panels loaded in compression and shear were summarized. The response and failure characteristics of specimens studied experimentally were described, and analytical and experimental results were compared. The specimens tested in the studies described were fabricated from commercially available 0.005-inch-thick unidirectional graphite-fiber tapes preimpregnated with 350 F cure thermosetting epoxy resins

    The general instability of eccentrically stiffened cylindrical shells under axial compression and lateral pressure

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    Instability of eccentrically stiffened cylindrical shells under axial compression and lateral pressur

    Short oestrous cycles in sheep during anoestrus involve defects in progesterone biosynthesis and luteal neovascularisation

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    Anoestrous ewes can be induced to ovulate by the socio-sexual, 'ram effect'. However, in some ewes the induced ovulation is followed by an abnormally short luteal phase causing a so called, "short cycle". The defect responsible for this luteal dysfunction has not been identified. In this experiment we investigated ovarian and uterine factors implicated in male-induced short cycles in anoestrus ewes using a combined endocrine and molecular strategy. Prior to ovulation, we were able to detect a moderate loss of thecal expression of steroid acute regulatory protein (STAR) in ewes that had not received progesterone priming (which prevents short cycles). At and following ovulation we were able to identify significant loss of expression of genes coding key proteins involved in the biosynthesis of progesterone (STAR, CYP11A1, HSD3B) as well as genes coding proteins critical for vascular development during early luteal development (VEGFA, VEGFR2) suggesting dysfunction in at least two pathways critical for normal luteal function. Furthermore, these changes were associated with a significant reduction of progesterone production and luteal weight. Additionally, we cast doubt on the proposed uterine-mediated effect of prostaglandin F2α as a cause of short cycles by demonstrating both the dysregulation of luteal expression of the PGF receptor, which mediates the luteal effects of PGF2α, and by finding no significant changes in the circulating concentrations of PGFM, the principal metabolite of PGF2α in ewes with short cycles. This study is the first of its kind to examine concurrently, the endocrine and molecular events in the follicular and early luteal stages of the short cycle

    A nucleotide sequence from a ribonuclease III processing site in bacteriophage T7 RNA.

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    Jump-like unravelings for non-Markovian open quantum systems

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    Non-Markovian evolution of an open quantum system can be `unraveled' into pure state trajectories generated by a non-Markovian stochastic (diffusive) Schr\"odinger equation, as introduced by Di\'osi, Gisin, and Strunz. Recently we have shown that such equations can be derived using the modal (hidden variable) interpretation of quantum mechanics. In this paper we generalize this theory to treat jump-like unravelings. To illustrate the jump-like behavior we consider a simple system: A classically driven (at Rabi frequency Ω\Omega) two-level atom coupled linearly to a three mode optical bath, with a central frequency equal to the frequency of the atom, ω0\omega_0, and the two side bands have frequencies ω0±Ω\omega_0\pm\Omega. In the large Ω\Omega limit we observed that the jump-like behavior is similar to that observed in this system with a Markovian (broad band) bath. This is expected as in the Markovian limit the fluorescence spectrum for a strongly driven two level atom takes the form of a Mollow triplet. However the length of time for which the Markovian-like behaviour persists depends upon {\em which} jump-like unraveling is used.Comment: 11 pages, 5 figure

    On Nichols algebras over PGL(2,q) and PSL(2,q)

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    We compute necessary conditions on Yetter-Drinfeld modules over the groups \mathbf{PGL}(2,q)=\mathbf{PGL}(2,\FF_q) and \mathbf{PSL}(2,q)=\mathbf{PSL}(2,\FF_q) to generate finite dimensional Nichols algebras. This is a first step towards a classification of pointed Hopf algebras with group of group-likes isomorphic to one of these groups. As a by-product of the techniques developed in this work, we prove that there is no non-trivial finite-dimensional pointed Hopf algebra over the Mathieu groups M20M_{20} and M21=PSL(3,4)M_{21}=\mathbf{PSL}(3,4).Comment: Minor change

    Functional rescue of dystrophin deficiency in mice caused by frameshift mutations using Campylobacter jejuni Cas9

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    Duchenne muscular dystrophy (DMD) is a fatal, X-linked muscle wasting disease caused by mutations in the DMD gene. In 51% of DMD cases, a reading frame is disrupted because of deletion of several exons. Here, we show that CjCas9 derived from Campylobacter jejuni can be used as a gene editing tool to correct an out-of-frame Dmd exon in Dmd knockout mice. Herein, we used Cas9 derived from S. pyogenes to generate Dmd knockout (KO) mice with a frameshift mutation in Dmd gene. Then, we expressed CjCas9, its single-guide RNA, and the eGFP gene in the tibialis anterior muscle of the Dmd KO mice using an all-in-one adeno-associated virus (AAV) vector. CjCas9 cleaved the target site in the Dmd gene efficiently in vivo and induced small insertions or deletions at the target site. This treatment resulted in conversion of the disrupted Dmd reading frame from out-of-frame to in-frame, leading to the expression of dystrophin in the sarcolemma. Importantly, muscle strength was enhanced in the CjCas9-treated muscles, without off-target mutations, indicating high efficiency and specificity of CjCas9. This work suggests that in vivo DMD frame correction, mediated by CjCas9 has great potential for the treatment of DMD and other neuromuscular diseases
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