ABSTRACT
In this paper, low circumferential reciprocating load foot-scale tests were performed on two nontruncated PHC B 600 130 tubular piles with bearing nodes to characterize the damage process and morphology of the specimens and to investigate the load-carrying performance of the members. The test results reveal that under the action of tensile-bending-shear loading, the bearing concrete in the node area buckles and is damaged, the anchored reinforcement in the node area yields, the constraint is weakened, an articulation point is formed, and the node rotational capacity increases. When the embedment depth increases from 200 mm to 300 mm, the ultimate bearing capacities of the positive and negative nodes increase by 31.04% and 36.16%, respectively. A numerical simulation is used to verify the test results. Considering the four types of piles without truncated nodes, the numerical simulation is used to analyze the node-bearing capacity at different embedment depths. Finally, a preferred node type is proposed as follows: a terminal plate welded anchor bar and pipe pile core-filled longitudinal reinforcement anchored into the bearing node, with a preferred embedment depth of 250 mm.
ABSTRACT
The nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces lung adenocarcinoma through formation of DNA adducts. Our previous research on susceptibility to tobacco-induced carcinogenesis focused on benzo[a]pyrene diol epoxide (BPDE) as the in vitro mutagen for phenotype measurements of DNA repair capacity (DRC) in mammalian cells. Here, we present a modified host-cell reactivation (HCR) assay to measure lymphocytic DRC for alkylating DNA damage as is induced by the tobacco-specific nitrosamine, NNK. We substituted dimethyl sulfate (DMS) to create alkylating damage in pCMVluc plasmid DNA and established the damage-repair dose-response curves in both normal and nucleotide excision repair-deficient lymphoblastoid cell lines and in phytohemagglutinin (PHA)-stimulated primary lymphocytes. We then successfully measured the DRC in PHA-stimulated lymphocytes from 48 patients with lung adenocarcinoma and 45 cancer-free controls and tested our hypothesis that lower DRC for alkylating damage is associated with an increased risk of lung adenocarcinoma. The cases exhibited a lower mean DRC than did the controls. A >3-fold increased risk (odds ratio = 3.21; 95% confidence interval = 1.25-8.21) was found for those with DRC levels below the control median. There was no correlation between the DRC measured with this DMS-HCR assay and that from the parallel BPDE-HCR assay. Interestingly, risk increased to >10-fold for those with sub-optimal DRC measured by both DMS- and BPDE-HCR assays. We conclude that variability in DRC is a risk factor for lung cancer and our results provide proof of principle for a new assay that can assess DRC for NNK-induced DNA damage.
