Analysis of flight delay and causal factors is crucial in maintaining airspace efficiency and safety. However, delay samples are not independent since they always show a certain aggregation pattern. Therefore, this study develops a novel spatial analysis approach to explore the delay and causal factors which is able to take dependence and the possible problem involved including error correlation and variable lag effect of causal factors on delay into account. The study first explores the delay aggregation pattern by measuring and quantifying the spatial dependence of delay. The spatial error model (SEM) and spatial lag model (SLM) are then established to solve the error correlation and the variable lag effect, respectively. Results show that the SEM and SLM achieve better fit than ordinary least square (OLS) regression, which indicates the effectiveness of considering dependence by employing spatial analysis. Moreover, the outcomes suggest that, aside from the well-known weather and flow control factors, delay-reduction strategies also need to pay more attention to reducing the impact of delay at the previous airport.
Surface-layer associated proteins (SLAP) of Lactobacillus paracasei ssp. paracasei M5-L and Lactobacillus casei Q8-L were examined to identify the functional basis for their protection within intestinal epithelial cells. The results showed that SLAP of M5-L and Q8-L remained active in a trypsin solution and retained a 45-kDa protein band, similar to that observed in controls. In contrast, under conditions of simulated gastric juice, the SLAP were partially degraded. Inhibitory effects of SLAP on adherence of Shigella sonnei to HT-29 cells were assessed with use of exclusion, competition, and replacement assays. In response to M5-L at 50 μg/mL SLAP, an inhibition ratio of 33% was obtained, while for Q8-L at 400 μg/mL SLAP, the inhibition ratio was 48%. Hoechst 33258 test results showed that cells infected with S. sonnei and co-incubated with SLAP of M5-L and Q8-L were only partially apoptotic, with apoptosis rates of 37.67 and 43.67%, respectively. These levels of apoptosis were substantially lower than that observed with cells infected with S. sonnei alone. In addition, the SLAP of Q8-L and M5-L reduced downstream caspase-1 activity and further modified apoptotic cell damage. Finally, SLAP of M5-L and Q8-L were also able to prevent S. sonnei-induced membrane damage by inhibiting delocalization of zonula occludens (ZO)-1 and reducing the amount of occludin produced by S. sonnei.
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