Embedded-ultrasonics structural radar (EUSR) is a new concept and methodology for in situ nondestructive evaluation (NDE) and structural health monitoring (SHM) of thin-wall structures. EUSR consists of: (a) an array of piezoelectric wafer active sensors (PWAS) embedded into the structure; and (b) electronic modules for signal transmission/reception, processing, and interpretation. EUSR utilizes guided elastic waves (Lamb waves) generated omnidirectionally into the thin-wall structure by surface-mounted permanently attached PWAS. The paper starts with the general concepts of the EUSR algorithm: transmission beamforming, reception beamforming, and time-of-fight (TOF) determination. Next, details of the Lamb wave generation with PWAS, verification of group-velocity dispersion curves, identification of optimal excitation frequency, and confirmation of wave front omnidirectionality are discussed. In the third part of the paper, the actual implementation of the EUSR method in a proof-of-concept demonstration is presented. The construction of the PWAS-phased array is described, and detection of cracks located broadside and offside of the PWAS array is illustrated. The method is shown to be easy to use through a visually interactive LabView TM interface. Very good detection accuracy is observed. The proof-of-concept experiments presented in this paper were illustrated on metallic structures; however, the EUSR concept may also work on composite and hybrid structures, although the range of detection may be reduced by the medium attenuation.

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this gene is not well investigated and the limited knowledge of this gene pointed to nervous system development. The chromosomal translocations in nervous development disorders usually lead to inactivation of this gene. In human tumours, both chromosomal deletion and translocation may also inactivate this gene and consequently contribute to tumorigenesis. Conclusions: We speculate that NKAIN2 could be a novel tumor suppressor on the 6q commonly deleted chromosomal region in human cancer and propose further researches required to investigate its potential tumor suppresser role. With the deepening of its involvement in human cancer and its cellular function, the role of NKAIN2 in tumorigenesis will be uncovered, which may impact the treatment of human malignancy. Cite this abstract as: Zhao S, Lian W, Luo F, Song X, Lv Y.Gonorrhea and prostate cancer incidence: an updated metaanalysis of 21 epidemiologic studies.

Piezoelectric wafer active sensors can be applied to aging aircraft structures to monitor the onset and progress of structural damage such as fatigue cracks and corrosion. Two main detection strategies are considered: (a) the wave propagation method for far-field damage detection; and (b) the electro-mechanical (E/M) impedance method for near-field damage detection. These methods are developed and verified on simple-geometry specimens, and then tested on realistic aging-aircraft panels with seeded cracks and corrosion. The specimens instrumentation with piezoelectric-wafer active sensors and ancillary apparatus is presented. The experimental methods, signal processing, and damage detection algorithms, tuned to the specific method used for structural interrogation, are discussed. In the wave propagation approach, the pulse-echo and acousto-ultrasonic methods were considered. Reflections from seeded cracks were successfully recorded. In addition, acoustic emission and low-velocity impact were also detected. In the E/M impedance method approach, the high-frequency spectrum is processed using overall-statistics damage metrics. The (1-R 2 ) 3 damage metric, where R is the correlation coefficient, was found to yield the best results. The simultaneous use of the E/M impedance method in the near field and of the wave propagation method in the far field opens the way for a comprehensive multifunctional damage detection system for aging aircraft structural health monitoring.

BackgroundDespite progress in treatment of small cell lung cancer (SCLC), the biology of the tumor still remains poorly understood. Recently, we globally investigated the contributions of lncRNA in SCLC with a special focus on sponge regulatory network. Here we report lncRNA HOTTIP, which is specifically amplified in SCLC, is associated with SCLC proliferation and poor prognosis of patients.MethodsRT-qPCR was used to investigate the expression of HOTTIP in SCLC tissues and cell lines. The role of HOTTIP in SCLC cell proliferation was demonstrated by CCK8 assay, colony formation assay, flow cytometry analysis and in vivo SCLC xenograft model in nude mice through HOTTIP loss- and gain-of-function effects. Western blot assay was used to evaluate gene expression in cell lines at protein level. RNA pull-down, Mass spectrometry and RNA binding protein immunoprecipitation (RIP) were performed to confirm the molecular mechanism of HOTTIP involved in SCLC progression.ResultsWe found that HOTTIP was overexpressed in SCLC tissues, and its expression was correlated with the clinical stage and the shorter survival time of SCLC patients. Moreover, HOTTIP knockdown could impair cell proliferation, affect the cell cycle and inhibit tumor growth of mice, while HOTTIP overexpression might enhance cell proliferation and cell cycle in vitro and in vivo. Mechanistic investigations showed that HOTTIP functions as an oncogene in SCLC progression by sponging miR-574-5p and affecting the expression of polycomb group protein EZH1.ConclusionsOverall, we identified that HOTTIP was involved in SCLC tumorigenesis through the ceRNA network “HOTTIP/miR-574-5p/EZH1”. Our findings not only illuminate how HOTTIP confers an oncogenic function in SCLC pathogenesis, but also underscore a novel gene expression governing hallmarks in the disease.Electronic supplementary materialThe online version of this article (10.1186/s12943-017-0729-1) contains supplementary material, which is available to authorized users.