Integrity Monitoring of Pressurized Gas Cylinders Using the SSUE Technique

Spread-Spectrum Ultrasonic Evaluation (SSUE) is a newly emerging technique for the global inspection and integrity monitoring of objects such as pressurized gas cylinders and structures such as bridges and airframes. This technique is based upon the measurement of an ultrasonic correlation signature which is sensitive to the structural and material properties of the test object. Recently, we applied the technique to pressurized gas cylinders and found that it was very sensitive to small changes in the cylinder. Specifically, we looked at the ability of the SSUE method to detect artificially-induced cracks at various points on the outside of the cylinder

Choice of Coded Waveform and Correlation Filter for Self-Noise Suppression in Ultrasonic Correlation Systems

Various ultrasonic correlation systems have been suggested in the past [1–5] in order to improve the flaw detection capability of ultrasonic NDE systems. These systems use a coded waveform for transmission, and the received signal is processed through a correlation filter. Although, these systems provide considerable improvement in the flaw detection capability, their performance is limited by what is called “self-noise” of the system. This paper discusses the self-noise limitation of conventional ultrasonic correlation systems and presents various approaches for self-noise suppression. Theoretically predicted performance has been verified using detailed computer simulations. Finally, comparison of the performance and practicability of each approach is discussed

Implementation of Self-Noise Suppression Techniques for Ultrasonic Correlation Systems

Pseudo-random signal correlation techniques can improve the flaw detection capability of ultrasonic NDE systems. While the correlation-based systems provide significant improvement in the signal-to-noise ratio compared to pulsed systems, their performance is limited by the so-called “self-noise” of the system. Self-noise is a result of imperfect autocorrelation characteristics of the excitation signal. Last year, we suggested some techniques for improving the flaw detection capability of continuous-mode ultrasonic NDE systems [1]. These systems use a continuously transmitted coded waveform as an excitation signal, and the received signal is processed through a correlation filter. This year, we present another new approach and demonstrate performance results and the practicability of each approach.</p

Imaging biomarker roadmap for cancer studies.

Imaging biomarkers (IBs) are integral to the routine management of patients with cancer. IBs used daily in oncology include clinical TNM stage, objective response and left ventricular ejection fraction. Other CT, MRI, PET and ultrasonography biomarkers are used extensively in cancer research and drug development. New IBs need to be established either as useful tools for testing research hypotheses in clinical trials and research studies, or as clinical decision-making tools for use in healthcare, by crossing 'translational gaps' through validation and qualification. Important differences exist between IBs and biospecimen-derived biomarkers and, therefore, the development of IBs requires a tailored 'roadmap'. Recognizing this need, Cancer Research UK (CRUK) and the European Organisation for Research and Treatment of Cancer (EORTC) assembled experts to review, debate and summarize the challenges of IB validation and qualification. This consensus group has produced 14 key recommendations for accelerating the clinical translation of IBs, which highlight the role of parallel (rather than sequential) tracks of technical (assay) validation, biological/clinical validation and assessment of cost-effectiveness; the need for IB standardization and accreditation systems; the need to continually revisit IB precision; an alternative framework for biological/clinical validation of IBs; and the essential requirements for multicentre studies to qualify IBs for clinical use.Development of this roadmap received support from Cancer Research UK and the Engineering and Physical Sciences Research Council (grant references A/15267, A/16463, A/16464, A/16465, A/16466 and A/18097), the EORTC Cancer Research Fund, and the Innovative Medicines Initiative Joint Undertaking (grant agreement number 115151), resources of which are composed of financial contribution from the European Union's Seventh Framework Programme (FP7/2007-2013) and European Federation of Pharmaceutical Industries and Associations (EFPIA) companies' in kind contribution

Absence of insulin signalling in skeletal muscle is associated with reduced muscle mass and function: evidence for decreased protein synthesis and not increased degradation

Loss of skeletal muscle mass and function is observed in many insulin-resistant disease states such as diabetes, cancer cachexia, renal failure and ageing although the mechanisms for this remain unclear. We hypothesised that impaired insulin signalling results in reduced muscle mass and function and that this decrease in muscle mass and function is due to both increased production of atrogenes and aberrant reactive oxygen species (ROS) generation. Maximum tetanic force of the extensor digitorum longus of muscle insulin receptor knockout (MIRKO) and lox/lox control mice was measured in situ. Muscles were removed for the measurement of mass, histological examination and ROS production. Activation of insulin signalling pathways, markers of muscle atrophy and indices of protein synthesis were determined in a separate group of MIRKO and lox/lox mice 15 min following treatment with insulin. Muscles from MIRKO mice had 36% lower maximum tetanic force generation compared with muscles of lox/lox mice. Muscle fibres of MIRKO mice were significantly smaller than those of lox/lox mice with no apparent structural abnormalities. Muscles from MIRKO mice demonstrated absent phosphorylation of AKT in response to exogenous insulin along with a failure to phosphorylate ribosomal S6 compared with lox/lox mice. Atrogin-1 and MuRF1 relative mRNA expression in muscles from MIRKO mice were decreased compared with muscles from lox/lox mice following insulin treatment. There were no differences in markers of reactive oxygen species damage between muscles from MIRKO mice and lox/lox mice. These data support the hypothesis that the absence of insulin signalling contributes to reduced muscle mass and function though decreased protein synthesis rather than proteasomal atrophic pathways