Compaction Grouting for Seismic Retrofit of the North Torrey Pines Bridge

The North Torrey Pines Road Bridge in Del Mar, California was built in 1933 and is eligible for listing in the National Register of Historic Places. As a result of its outdated design and deterioration in a corrosive saline environment, the bridge was classified as structurally and seismically deficient and functionally obsolete. The historic significance of this bridge is important to the surrounding community and thus a seismic retrofit project was initiated with the goal of improving the expected seismic performance of the bridge while preserving its aesthetic and historic character. This paper provides a brief description of the overall retrofit design strategy, and detailed descriptions of the design of compaction grouting ground improvement to mitigate liquefaction and seismic slope instability hazards. Techniques used in the compaction grouting construction are presented, along with some particular construction challenges and solutions. Pre- and post-construction Standard Penetration Test data are compared and the improvements to the soil are discussed. The compaction grouting program was successful in achieving the ground improvement levels required by the design

General Report - Session 6

This general report provides a summary of 40 accepted papers submitted to sessions 6a on ground improvement methods and session 6b on geoenvironmental engineering. The papers are contributed by the researchers and professionals from the United States and 15 other countries and they cover a wide range of topics based on laboratory experiments, field design, construction and monitoring, and mathematical modeling. A brief summary of each paper is provided under organized sections and the reader is referred to consult the full paper for details. Finally, the topics for discussion are listed

Evaluation of a geogrid-reinforced soil mat to mitigate post-liquefaction settlements - A case study

The use of geogrid reinforced soil mats has become a viable method to mitigate differential settlements caused by deformations in the underlying soils, including those resulting from fault rupture and seismically induced settlements. In this paper a case study is presented where numerical modeling was used to evaluate the effectiveness of geogrid reinforced soil to mitigate as much as 100 mm of differential seismic settlement. The subsurface investigation, which made extensive use of the cone penetration test, is first presented. Using this information, numerical models were then developed. Descriptions of the modeling procedures are presented and important/sensitive aspects of the models are discussed. The results of the modeling are presented and observations are made regarding performance of the geogrid-reinforced soil system. Areas where additional studies are warranted are identified. © 2008 ASCE

Fault Hazard Characterization for a Transportation Tunnel Project in Coronado, California

This paper presents the results of a fault hazard study performed as part of a proposed traffic tunnel project in Coronado, California. The 2.3 km alignment crosses the Coronado fault, which is considered active by the California Geological Survey. Although the location of the Coronado fault offshore of Coronado had been well established through previous studies, the fault had never been definitively located on land. A study was undertaken that utilized four principal investigation methods: a seismic reflection survey, large diameter borings, closely-spaced cone penetrometer tests (CPT) and a fault trench. This study was the first to positively locate the Coronado fault on land and to show that approximately 29 cm of vertical displacement has occurred in the Holocene. The field investigation provided evidence that strike slip displacement has also occurred. For design purposes, the strike slip offset was estimated using an empirical model and several kinematic models that integrated aspects of the local tectonic regime. Fault offset design criteria were established for the project that accounted for uncertainty in the fault zone location and the potential for secondary faulting outside the primary fault zone

Endoxifen’s Molecular Mechanisms of Action Are Concentration Dependent and Different than That of Other Anti-Estrogens

<div><p>Endoxifen, a cytochrome P450 mediated tamoxifen metabolite, is being developed as a drug for the treatment of estrogen receptor (ER) positive breast cancer. Endoxifen is known to be a potent anti-estrogen and its mechanisms of action are still being elucidated. Here, we demonstrate that endoxifen-mediated recruitment of ERα to known target genes differs from that of 4-hydroxy-tamoxifen (4HT) and ICI-182,780 (ICI). Global gene expression profiling of MCF7 cells revealed substantial differences in the transcriptome following treatment with 4HT, endoxifen and ICI, both in the presence and absence of estrogen. Alterations in endoxifen concentrations also dramatically altered the gene expression profiles of MCF7 cells, even in the presence of clinically relevant concentrations of tamoxifen and its metabolites, 4HT and N-desmethyl-tamoxifen (NDT). Pathway analysis of differentially regulated genes revealed substantial differences related to endoxifen concentrations including significant induction of cell cycle arrest and markers of apoptosis following treatment with high, but not low, concentrations of endoxifen. Taken together, these data demonstrate that endoxifen’s mechanism of action is different from that of 4HT and ICI and provide mechanistic insight into the potential importance of endoxifen in the suppression of breast cancer growth and progression.</p> </div

Profile of cell cycle changes induced by endoxifen.

<p>MCF7 cells were treated as indicated for 24 hours and cell cycle profiles were determined by propidium iodide staining and flow cytometry. (<b>A</b>) The percentage of cells from each treatment in G2/M phase (blue), S phase (green) and G1 phase (red) are shown. Asterisks within each cell cycle phase denote significance at the P<0.05 level (ANOVA) compared to vehicle controls. # within each cell cycle phase denotes significant differences (P<0.05) compared to estrogen treated cells. (<b>B</b>) Representative flow cytometry plots for each treatment condition.</p

Biological pathways detected to be significantly regulated based upon endoxifen concentrations under physiologically relevant conditions.

<p>Biological pathways detected to be significantly regulated based upon endoxifen concentrations under physiologically relevant conditions.</p

Venn diagrams depicting the anti-estrogen specific effects on estrogen-dependent and -independent genes.

<p>(<b>A</b>) Venn of genes whose expression levels were significantly altered by 1.5 fold or greater in MCF7 cells treated with 10 nM estrogen plus 100 nM concentrations of indicated anti-estrogens, relative to cells treated with estrogen alone following 24 hours of exposure. (<b>B</b>) Venn diagram of genes whose expression levels were significantly altered by 1.5 fold or greater in MCF7 cells treated with 10 nM estrogen plus 100 nM concentrations of indicated anti-estrogens, but not by estrogen treatment alone, relative to vehicle treated controls following 24 hours of exposure.</p

ChIP analysis of ERα binding to a consensus ERE and endogenous target genes.

<p>ChIP assays were performed in MCF7 cells transiently transfected with a consensus ERE and treated as indicated for either 1 hour (<b>A</b>) or 24 hours (<b>B</b>). Data are expressed as the relative abundance of the target following indicated treatments relative to vehicle treated controls as detected by real-time PCR. All data were normalized using input values. Experiments were conducted in triplicate and a representative data set is shown. Asterisks denote significance at the P<0.05 level (ANOVA) compared to vehicle controls. # denotes significant differences (P<0.05) between estrogen and anti-estrogen treatments.</p

Real-time PCR confirmation of selected genes whose expression levels were either increased (red) or decreased (green) by a specific anti-estrogen.

<p>Genes whose expression levels were determined to be specifically increased (red) or decreased (green) by only one of the three anti-estrogen treatments were randomly selected for confirmation of the microarray data. Darkly shaded bars depict relative fold changes from vehicle treated cells (dashed line) as detected by microarray analysis while lightly shaded bars depict fold change as detected by RT-PCR analysis. Solid lines represent the 1.5 fold cut-off used in the microarray analysis. Data represent the mean ± the standard error of three independent treatments. Asterisks denote values with significant differences at the P<0.05 level (ANOVA) relative to vehicle treated controls which also met the 1.5 fold cut-off parameter used in the microarray analysis.</p