Development of Features for Early Detection of Defects and Assessment of Bridge Decks

Damage detection is an important area with growing interest in mechanical and structural engineering.One of the critical issues in damage detection is how to determine indices sensitive to the structural damage and insensitive to the surrounding environmental variations.Current damage identification indices commonly focus on structural dynamic characteristics such as natural frequencies,mode shapes,and frequency responses.This study aimed at developing a technique based on energy Curvature Difference,power spectrum density,correlation-based index,load distribution factor,and neutral axis shift to assess the bridge deck condition.In addition to tracking energy and frequency over time using wavelet packet transform,in order to further demonstrate the feasibility and validity of the proposed technique for bridge condition assessment,experimental strain data measured from two stages of a bridge in the different intervals were used.The comparative analysis results of the bridge in first and second stage show changes in the proposed feature values.It is concluded,these changes in the values of the proposed features can be used to assess the bridge deck performance.

Bisphenol A exposure alters release of immune and developmental modulators and expression of estrogen receptors in human fetal lung fibroblasts

Bisphenol A （BPA） has been shown to exert biological effects through estrogen receptor （ER）-dependent and ER-independent mechanisms. Recent studies suggest that prenatal exposure to BPA may increase the risk of childhood asthma. To investigate the underlying mechanisms in the actions of BPA, human fetal lung fibroblasts {hFLFs） were exposed to varying doses of BPA in culture for 24 hr. Effects of BPA on localization and uptake of BPA, cell viability, release of immune and developmental modulators, cellular localization and expression of ERa, ERβ and G-protein coupled estrogen receptor 30 （GPR30）, and effects of ERs antagonists on BPA-induced changes in endothelin-1 （ET-1） release were examined. BPA at 0.01-100 μmol/L caused no changes in cell viability after 24 hr of exposure, hFLFs expresses all three ERs. BPA had no effects on either cellular distribution or protein expression of ERa, however, at 100 μmol/L （or 23 μmol/L intracellular BPA） increased ERβ protein levels in the cytoplasmic fractions and GPR30 protein levels in the nuclear fractions. These paralleled with increased release of growth differentiation factor-15, decreased phosphorylation of nuclear factor kappa B p65 at serine 536, and decreased release of ET-1, interleukin-6, and interferon gamma-induced protein 10. ERs antagonists had no effects on BPA-induced decrease in ET-1 release. These data suggest that BPA at 100 μmol/L altered the release of immune and developmental modulators in hFLFs, which may negatively influence fetal lung development, maturation, and susceptibility to environmental stressors, although the role of BPA in childhood asthma remains to be confirmed in in viuo studies.

RCAN family member 3 deficiency contributes to noncompaction of the ventricular myocardium

Noncompaction of the ventricular myocardium(NVM),the third most diagnosed cardiomyopathy,is characterized by prominent trabeculae and intratrabecular recesses.However,the genetic etiology of 40%–60%of NVM cases remains unknown.Here,we identify two infants with NVM,in a nonconsanguineous family,with a typical clinical presentation of persistent bradycardia since the prenatal period.A homozygous missense variant(R223L)of RCAN family member 3(RCAN3)is detected in both infants using whole-exome sequencing.In the zebrafish model,marked cardiac dysfunction is detected in rcan3 deficiency(MO-rcan3^(ATG)-injected)and rcan^(−/−) embryos.Developmental dysplasia of both endocardial and myocardial layers is also detected in rcan3-deficient embryos.RCAN3 R223L variant mRNAs can not rescue heart defects caused by rcan3 knockdown or knockout;however,hRCAN3 mRNAs rescue these phenotypes.RNA-seq experiments show that several genes involved in cardiomyopathies are significantly regulated through multiple signaling pathways in the rcan3-knockdown zebrafish model.In human cardiomyocytes,RCAN3 deficiency results in reduced proliferation and increased apoptosis,together with an abnormal mitochondrial ultrastructure.Thus,we suggest that RCAN3 is a susceptibility gene for cardiomyopathies,especially NVM and that the R223L mutation is a potential loss-of-function variant.