用测量模态阻尼和振型的方法对复合材料薄平板进行无损质量检测

复合材料薄平板经热压制成后,都需要进行质量检测。本文探索用测量模态阻尼和振型的方法,对复合材料薄平板的制作质量进行无损检测,作为对其它昂贵的无损检测方法的补充。略述用振动方法进行无损检测的原理,测量薄平板阻尼的方法以及提高测量精度的措施。还讨论在测量薄平板阻尼时可能遇到的一些特殊问题(如非线性刚度、拍、模态密集等问题);以云母基复合材料薄平板作为例子,从测量其阻尼和振型的结果,对这种板的制作质量进行讨论。     

考虑轴颈偏斜时滑动轴承的动力特性

本文建立了同时考虑轴颈径向位移和歪斜时的滑动轴承动力学模型.对于这种模型,油膜力将扩展为四个广义力分量.文章将相应的动力系数矩阵分解为对称和反对称两部分并讨论其物理性质.然后,本文推导得出该模型的正交变换矩阵,在此基础上导得各向同性的动力系数矩阵表达式,并讨论了诸元素的物理意义.文章最后引入动力系数椭圆的概念以分析非对称动力系数矩阵的变换性质.     

美国

美国,凭借其幅员辽阔的疆域、在研究及发展上持续不断的投入以及高质量的教育系统,自Vannevar Bush起草并发表了具有深远影响且备受推崇的讨论美国战后科学政策的报告《科学,无止境的前沿》(Science,TheEndless Frontier)[1]之时起,美国这个国家在世界科学领域就一直占据主导地位.然而进入21...     

Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disorder resulting from motor neuron death. Approximately 10% of cases are familial (FALS), typically with a dominant inheritance mode. Despite numerous advances in recent years, nearly 50% of FALS cases have unknown genetic aetiology. Here we show that mutations within the profilin 1 (PFN1) gene can cause FALS. PFN1 is crucial for the conversion of monomeric (G)-actin to filamentous (F)-actin. Exome sequencing of two large ALS families showed different mutations within the PFN1 gene. Further sequence analysis identified 4 mutations in 7 out of 274 FALS cases. Cells expressing PFN1 mutants contain ubiquitinated, insoluble aggregates that in many cases contain the ALS-associated protein TDP-43. PFN1 mutants also display decreased bound actin levels and can inhibit axon outgrowth. Furthermore, primary motor neurons expressing mutant PFN1 display smaller growth cones with a reduced F/G-actin ratio. These observations further document that cytoskeletal pathway alterations contribute to ALS pathogenesis.     

Proxy evidence for an El Niño-like response to volcanic forcing

Past studies have suggested a statistical connection between explosive volcanic eruptions and subsequent El Ni?o climate events. This connection, however, has remained controversial. Here we present support for a response of the El Ni?o/Southern Oscillation (ENSO) phenomenon to forcing from explosive volcanism by using two different palaeoclimate reconstructions of El Ni?o activity and two independent, proxy-based chronologies of explosive volcanic activity from ad 1649 to the present. We demonstrate a significant, multi-year, El Ni?o-like response to explosive tropical volcanic forcing over the past several centuries. The results imply roughly a doubling of the probability of an El Ni?o event occurring in the winter following a volcanic eruption. Our empirical findings shed light on how the tropical Pacific ocean-atmosphere system may respond to exogenous (both natural and anthropogenic) radiative forcing.     

Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF-VEGFR2 signalling

Developing tissues and growing tumours produce vascular endothelial growth factors (VEGFs), leading to the activation of the corresponding receptors in endothelial cells. The resultant angiogenic expansion of the local vasculature can promote physiological and pathological growth processes. Previous work has uncovered that the VEGF and Notch pathways are tightly linked. Signalling triggered by VEGF-A (also known as VEGF) has been shown to induce expression of the Notch ligand DLL4 in angiogenic vessels and, most prominently, in the tip of endothelial sprouts. DLL4 activates Notch in adjacent cells, which suppresses the expression of VEGF receptors and thereby restrains endothelial sprouting and proliferation. Here we show, by using inducible loss-of-function genetics in combination with inhibitors in vivo, that DLL4 protein expression in retinal tip cells is only weakly modulated by VEGFR2 signalling. Surprisingly, Notch inhibition also had no significant impact on VEGFR2 expression and induced deregulated endothelial sprouting and proliferation even in the absence of VEGFR2, which is the most important VEGF-A receptor and is considered to be indispensable for these processes. By contrast, VEGFR3, the main receptor for VEGF-C, was strongly modulated by Notch. VEGFR3 kinase-activity inhibitors but not ligand-blocking antibodies suppressed the sprouting of endothelial cells that had low Notch signalling activity. Our results establish that VEGFR2 and VEGFR3 are regulated in a highly differential manner by Notch. We propose that successful anti-angiogenic targeting of these receptors and their ligands will strongly depend on the status of endothelial Notch signalling.     

Coherent control of pulsed X-ray beams.

Synchrotrons produce continuous trains of closely spaced X-ray pulses. Application of such sources to the study of atomic-scale motion requires efficient modulation of these beams on timescales ranging from nanoseconds to femtoseconds. However, ultrafast X-ray modulators are not generally available. Here we report efficient subnanosecond coherent switching of synchrotron beams by using acoustic pulses in a crystal to modulate the anomalous low-loss transmission of X-ray pulses. The acoustic excitation transfers energy between two X-ray beams in a time shorter than the synchrotron pulse width of about 100 ps. Gigahertz modulation of the diffracted X-rays is also observed. We report different geometric arrangements, such as a switch based on the collision of two counter-propagating acoustic pulses: this doubles the X-ray modulation frequency, and also provides a means of observing a localized transient strain inside an opaque material. We expect that these techniques could be scaled to produce subpicosecond pulses, through laser-generated coherent optical phonon modulation of X-ray diffraction in crystals. Such ultrafast capabilities have been demonstrated thus far only in laser-generated X-ray sources, or through the use of X-ray streak cameras.