115 research outputs found

    Preface

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    Origin of Spurious Ultrasonic Echoes in Stainless Steel Piping with Weld Overlay

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    The initiation and growth of intergranular stress-corrosion cracking (IGSCC) in the heat-affected zone of welds in stainless steel reactor piping has been a subject of concern to electric utilities for over ten years. This type of crack can be detected with ultrasonic shear waves during normal maintenance periods with a reliability of up to 80% [1]. Often, when crack indications have been found, the utility has been allowed to apply a weld metal overlay as a temporary repair measure. However, the complex, elastically anisotropic microstructure of the overlay considerably reduces the reliability of subsequent ultrasonic inspections. This paper addresses the problems arising because of the overlay

    Analytic Diffraction Corrections to Ultrasonic Scattering Measurements

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    Ultrasonic theories generally predict a scattering amplitude which relates a spherically spreading, far-field scattered wave to an incident plane wave. In ultrasonic immersion measurements, the frequency and angular dependences of the scattering amplitude are convolved with those of the transmitting and receiving transducers and the propagation through the liquid-solid and solid-liquid interfaces. This paper presents a set of approximate corrections for these effects for the cases of angle beam inspection through planar, spherically curved or cylindrically curved surfaces. The primary parameters in the correction are the function D, which corrects for the diffraction effects occurring during a transducer calibration experiment, and the function C, which describes the on-axis pressure variation of the beam. Values of C and D are available in the literature for the case of a piston transducer radiating into an infinite fluid medium. The major portion of this paper is concerned with the extension of those results to the aforementioned two media problems in which mode conversion, refraction, diffraction, and focussing all play interrelated roles. Results of preliminary experiments to test the corrections are also included

    Chloroquine activates the p53 pathway and induces apoptosis in human glioma cells

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    Glioblastoma is the most common malignant brain tumor in adults. The currently available treatments offer only a palliative survival advantage and the need for effective treatments remains an urgent priority. Activation of the p53 growth suppression/apoptotic pathway is one of the promising strategies in targeting glioma cells. We show that the quinoline derivative chloroquine activates the p53 pathway and suppresses growth of glioma cells in vitro and in vivo in an orthotopic (U87MG) human glioblastoma mouse model. Induction of apoptosis is one of the mechanisms underlying the effects of chloroquine on suppressing glioma cell growth and viability. siRNA-mediated downregulation of p53 in wild-type but not mutant p53 glioblastoma cells substantially impaired chloroquine-induced apoptosis. In addition to its p53-activating effects, chloroquine may also inhibit glioma cell growth via p53-independent mechanisms. Our results clarify the mechanistic basis underlying the antineoplastic effect of chloroquine and reveal its therapeutic potential as an adjunct to glioma chemotherapy
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