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This paper presents damage identification of a full-scale, five-girder bridge subjected to controlled levels of sequential damage using time-series analysis of vibration data measured during field tests and also simulated by finite-element (FE) modeling.
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Differentiating the damages into various levels and analyzing the percentage of damage to the cells showed that photocatalysis was likely to elicit sequential damages in E. coli cells.
Among them, miR-340-5p, miR-484, miR-720-3p, miR-720, whose expression was never described in NAFLD, NASH and HCC tissues, and miR-125a-5p miR-125a-5p miR-125a-5ped eandy and significant dysregulation in the sequential hepatic damage process.
In this study, sequential approaches for damage detection in beams using time-modal features and artificial neural networks are proposed.
This too can be posited in the context of the multiple-hit hypothesis described previously, in that sequential and permanent damage to different target sites within the system could also result in compromise of homeostatic regulatory capacities.
Results showed that the TO-treated samples offered the best resistance to the sequential actions of mechanical damage (simulated abrasion) and corrosion.
It is shown that the unloading response consists of five sequential stages: elastic recovery, interface damage (crack) initiation, damage evolution (delamination), film elastic bending, and abrupt surface separation (jump-out), with plastic deformation in the substrate occurring only during damage initiation.
Recently, a new damage indicator-based sequential law has been proposed to capture the load sequence effect more precisely.
When sequential indentations are considered, the damage tends to accumulate in a central region in between the two indentations and the severity of damage is significantly higher.
There was also significantly less radiographically determined damage than with sequential monotherapy or step-up therapy.
The progressive accumulation of DNA damage with each sequential cell cycle has been considered to be the primary cause of cell aging and senescence [ 20].
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