3,418 research outputs found

    Crack identification of functionally graded beams using continuous wavelet transform

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    © 2018 Elsevier Ltd This paper proposes a new damage index for the crack identification of beams made of functionally graded materials (FGMs) by using the wavelet analysis. The damage index is defined based on the position of the wavelet coefficient modulus maxima in the scale space. The crack is assumed to be an open edge crack and is modeled by a massless rotational spring. It is assumed that the material properties follow exponential distributions along the beam thickness direction. The Timoshenko beam theory is employed to derive the governing equations which are solved analytically to obtain the frequency and mode shape of cracked FGM beams. Then, we apply the continuous wavelet transform (CWT) to the mode shapes of the cracked FGM beams. The locations of the cracks are determined from the sudden changes in the spatial variation of the damage index. An intensity factor, which relates to the size of the crack and the coefficient of the wavelet transform, is employed to estimate the crack depth. The effects of the crack size, the crack location and the Young's modulus ratio on the crack depth detection are investigated

    Alternative Splicing of P/Q-Type Ca2+ Channels Shapes Presynaptic Plasticity

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    Alternative splicing of pre-mRNAs is prominent in the mammalian brain, where it is thought to expand proteome diversity. For example, alternative splicing of voltage-gated Ca2+ channel (VGCC) α1 subunits can generate thousands of isoforms with differential properties and expression patterns. However, the impact of this molecular diversity on brain function, particularly on synaptic transmission, which crucially depends on VGCCs, is unclear. Here, we investigate how two major splice isoforms of P/Q-type VGCCs (Cav2.1[EFa/b]) regulate presynaptic plasticity in hippocampal neurons. We find that the efficacy of P/Q-type VGCC isoforms in supporting synaptic transmission is markedly different, with Cav2.1[EFa] promoting synaptic depression and Cav2.1[EFb] synaptic facilitation. Following a reduction in network activity, hippocampal neurons upregulate selectively Cav2.1[EFa], the isoform exhibiting the higher synaptic efficacy, thus effectively supporting presynaptic homeostatic plasticity. Therefore, the balance between VGCC splice variants at the synapse is a key factor in controlling neurotransmitter release and presynaptic plasticity

    Faint young Sun paradox remains

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    The Sun was fainter when the Earth was young, but the climate was generally at least as warm as today; this is known as the `faint young Sun paradox'. Rosing et al. [1] claim that the paradox can be resolved by making the early Earth's clouds and surface less reflective. We show that, even with the strongest plausible assumptions, reducing cloud and surface albedos falls short by a factor of two of resolving the paradox. A temperate Archean climate cannot be reconciled with the low level of CO2 suggested by Rosing et al. [1]; a stronger greenhouse effect is needed.Comment: 3 pages, no figures. In press in Nature. v2 corrects typo in author list in original submissio

    Independent regulation of Basal neurotransmitter release efficacy by variable Ca²+ influx and bouton size at small central synapses.

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    The efficacy of action potential evoked neurotransmitter release varies widely even among synapses supplied by the same axon, and the number of release-ready vesicles at each synapse is a major determinant of this heterogeneity. Here we identify a second, equally important, mechanism for release heterogeneity at small hippocampal synapses, the inter-synaptic variation of the exocytosis probability of release-ready vesicles. Using concurrent measurements of vesicular pool sizes, vesicular exocytosis rates, and presynaptic Ca²⁺ dynamics, in the same small hippocampal boutons, we show that the average fusion probability of release-ready vesicles varies among synapses supplied by the same axon with the size of the spike-evoked Ca²⁺ concentration transient. We further show that synapses with a high vesicular release probability exhibit a lower Ca²⁺ cooperativity, arguing that this is a direct consequence of increased Ca²⁺ influx at the active zone. We conclude that variability of neurotransmitter release under basal conditions at small central synapses is accounted for not only by the number of release-ready vesicles, but also by their fusion probabilities, which are set independently of bouton size by variable spike-evoked presynaptic Ca²⁺ influx

    Viral Envelope Protein 53R Gene Highly Specific Silencing and Iridovirus Resistance in Fish Cells by AmiRNA

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    BACKGROUND: Envelope protein 53R was identified from frog Rana grylio virus (RGV), a member of the family Iridoviridae, and it plays an important role in the virus assembly. Although inhibition of iridovirus major capsid protein (MCP) by small hairpin RNAs (shRNAs) has been shown to cause resistance to viral infection in vitro, RNA interference (RNAi) to inhibit aquatic animal virus envelope protein gene product has not been reported. METHODOLOGY: We devised artificial microRNAs (amiRNAs) that target a viral envelope protein gene RGV 53R. By incorporating sequences encoding amiRNAs specific to 53R of RGV into pre-miRNA155 (pSM155) vectors, which use the backbone of natural miR-155 sequence and could intracellularly express 53R-targeted pre-amiRNAs. The pre-amiRNAs could be processed by the RNase III-like enzyme Dicer into 21-25 nt amiRNAs (amiR-53Rs) in fish cell lines. The levels of 53R expression were analyzed through real-time PCR and RGV virions assembly were observed by electronic microscopy in fish cells transfected with or without amiR-53Rs at 72 h of RGV infection. CONCLUSION/SIGNIFICANCE: The results argue that viral envelope protein RGV 53R can be silenced and the virions assembly was deficient by amiR-53R-1, and further identified the first amiRNA of envelope protein gene from iridovirus that was able to cause resistance to virus infection in fish cells. The data demonstrate that the viral infection is efficiently suppressed (58%) by amiR-53R-1 targeting positon 36-57 of RGV 53R. Moreover, electron microscopic observations revealed virion assembly defect or reduced virions assembly capacity was closely correlated to expression of amiR-53R-1. Based on real time PCR of the Mx gene, we found no evidence of activation of IFN by amiR-53R-1

    Oscillations and interactions of dark and dark-bright solitons in Bose-Einstein condensates

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    Solitons are among the most distinguishing fundamental excitations in a wide range of non-linear systems such as water in narrow channels, high speed optical communication, molecular biology and astrophysics. Stabilized by a balance between spreading and focusing, solitons are wavepackets, which share some exceptional generic features like form-stability and particle-like properties. Ultra-cold quantum gases represent very pure and well-controlled non-linear systems, therefore offering unique possibilities to study soliton dynamics. Here we report on the first observation of long-lived dark and dark-bright solitons with lifetimes of up to several seconds as well as their dynamics in highly stable optically trapped 87^{87}Rb Bose-Einstein condensates. In particular, our detailed studies of dark and dark-bright soliton oscillations reveal the particle-like nature of these collective excitations for the first time. In addition, we discuss the collision between these two types of solitary excitations in Bose-Einstein condensates.Comment: 9 pages, 4 figure

    Long-term safety and outcome of a temporary self-expanding metallic stent for achalasia: a prospective study with a 13-year single-center experience

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    To prospectively evaluate the long-term clinical safety and efficacy of a newly designed self-expanding metallic stent (SEMS) in the treatment of patients with achalasia. Seventy-five patients with achalasia were treated with a temporary SEMS with a 30-mm diameter. The SEMSs were placed under fluoroscopic guidance and removed by gastroscopy 4–5 days after stent placement. Follow-up data focused on dysphagia score, technique and clinical success, clinical remissions and failures, and complications and was performed at 6 months, 1 year, and within 3 to 5 years, 5 to 8 years, 8 to 10 years, and >10 years postoperatively. Stent placement was technically successful in all patients. Complications included stent migration (n = 4, 5.33%), chest pain (n = 28, 38.7%), reflux (n = 15, 20%), and bleeding (n = 9, 12%). No perforation or 30-day mortality occurred. Clinical success was achieved in all patients 1 month after stent removal. The overall remission rates at 6 months, 1, 1–3, 3–5, 5–8, 8–10, and >10 year follow-up periods were 100%, 96%, 93.9%, 90.9%, 100%, 100%, and 83.3%, respectively. Stent treatment failed in six patients, and the overall remission rate in our series was 92%. The median and mean primary patencies were 2.8 ± 0.28 years (95% CI: 2.25–3.35) and 4.28 ± 0.40 years (95% CI: 3.51–5.05), respectively. The use of temporary SEMSs with 30-mm diameter proved to be a safe and effective approach for managing achalasia with a long-term satisfactory clinical remission rate
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