SAFETY ASSESSMENT OF CONTINUOUS CONCRETE GIRDER BRIDGES SUBJECTED TO RANDOM TRAFFIC LOADS CONSIDERING FLEXURAL-SHEAR COUPLED FAILURE

Bridges generally perform complicated mechanical behaviors under external loads, such as flexural-shear coupling, compression-bending coupling, and flexural-shear-torsion coupling. In the context of deterministic design approaches such as design codes, these complicated coupled issues are generally simplified to the safety verification of bridge components under a single mechanical state (i.e. flexural, shear, torsion). At present, the rapid development of sensor and information technologies makes it possible to collect the external loads acted on bridges and understand bridge performance under these stochastic external loads. In this manner, the reliability-based full probabilistic approach could be applied to investigate the performance of bridges over their lifetime. However, the current bridge reliability assessment incorporating realistic traffic load measurements mainly focuses on the analysis of bridge components under a single mechanical state. In this paper, a reliability-based probabilistic analytical framework of the flexural-shear performance of girder bridges under random traffic loading is established. The flexural-shear coupled failure path of bridge girders under random traffic loading is characterized for the first time, where the bivariate extreme value theory is incorporated to develop the extreme value distribution of combined flexural and shear load effects. The modified compression field theory recommended by AASHTO is employed to establish the coupled flexural-shear coupling resistances. Finally, the reliability of the flexural-shear performance of bridge girders is evaluated by solving the multivariate ultimate limit state equation. The proposed analytical framework is applied to a realistic bridge. The results show that the reliability index of the flexural-shear coupling evaluation is lower than that of the flexural or shear evaluation, which highlights the importance of the flexural-shear performance checking in the reliability assessment of bridges under random traffic loading. The proposed analytical framework could be further applied to the probabilistic assessment of bridge components subjected to combined loading mechanisms under random loadings

Protective Role of Hepassocin against Hepatic Endoplasmic Reticulum Stress in Mice

Hepassocin (HPS) is a hepatokine that has multiple proposed physiological functions. Some of the biological processes in which it is involved are closely related to endoplasmic reticulum (ER) stress, but the role of HPS in the regulation of ER stress remains unclear. Here, we demonstrated that HPS transcription is induced by the protein kinase RNA-like ER kinase (PERK)/activating transcription factor 4 (ATF4) cascade upon ER stress in hepatocytes. Additionally, fasting/refeeding also induced HPS expression in mice liver. The loss of HPS sensitizes hepatocytes to ER stress-related cytotoxicity in vitro, whereas HPS treatment altered these phenotypes. HPS deficiency exacerbates fasting/refeeding-induced ER stress in vivo. The preliminary administration of HPS ameliorates liver steatosis, cell death, and inflammation in mice injected with tunicamycin (TM). The improvement of HPS can be observed even if HPS protein is injected after TM treatment. Furthermore, the administration of an ER stress inhibitor alleviated steatohepatitis in methionine- and choline-deficient (MCD) diet-fed HPS-deficient mice. These results suggest that HPS protects hepatocytes from physiological and pathological ER stress, and that the inactivation of HPS signaling aggravating ER stress may be a novel mechanism that drives the development of steatohepatitis. The protective mechanism of HPS against ER stress in hepatocytes was associated with the regulation of ER calcium handling, and the suppression of calcium influx release from ER upon stressor treatment. Collectively, our findings indicate that HPS may act in a negative feedback fashion to regulate hepatic ER stress and protect hepatocytes from ER stress-related injury. HPS has the potential to be a candidate drug for the treatment of ER stress-related liver injury