11 research outputs found

    Tectonic evolution and midplate volcanism in the South Pacific

    Get PDF
    Thesis (Ph.D.)--Joint Program in Oceanography, Massachusetts Institute of Technology/Woods Hole Oceanographic Institution, 1999.Includes bibliographical references (leaves 131-139).by Kelsey Allyn Jordahl.Ph.D

    Why there Are no Earthquakes on the Marquesas Fracture Zone

    No full text
    Although the plate tectonic paradigm does not predict relative horizontal motion between lithosphere on opposing sides of a fracture zone, the fact that younger, more rapidly subsiding seafloor lies adjacent to older seafloor implies relative vertical motion. The observation that fracture zones are notably aseismic has led to the proposition of high strength along fracture zones, such that the differential subsidence is accommodated by flexure across a locked fault. This model predicts that a ridge develops on the young side of the fracture zone flanked by a foredeep trough on the old side, with parallel warping of the Moho and large associated gravity anomalies. Previous analyses of satellite altimetric passes over Pacific fracture zones have shown that the amplitude and shape of the gravity anomalies frequently do not conform to the predictions of this simple model. One of the most notable departures has been the Marquesas Fracture Zone (MFZ), where only one limited section was determined to be “high strength.” Curiously, the only earthquake to rupture the MFZ in the last 35 years is located in this locked region. Elsewhere, where we would predict vertical slip must be occurring, the fault is aseismic. To better understand the history of vertical motion on this fault, we have analyzed geophysical data obtained during the recent survey EW9106 aboard the R/V Maurice Ewing. Our detailed Hydrosweep, gravity, and seismic data resolve this paradox by showing no evidence for vertical slip along the fault. Shear stresses caused by differential thermal subsidence do not exceed the strength of this fault. Rather, the failure of the altimetry signal to conform to the predictions of the high-strength model along much of the MFZ is caused by changes in the Pacific-Farallon pole of rotation. Reorientation of the plate boundary was accommodated by propagating rifts, intratransform tension or compression, and changes in transform offset that complicated the signal from differential subsidence across a locked fault. For example, a counterclockwise rotation of the transform in the Cretaceous caused overthrusting in the transform and thus compensation of the depth differential by flexural loading of a very young plate. A clockwise rotation of this right-stepping transform fault at about 35 Ma led temporarily to a crenulated plate boundary and later to the development of intra-transform spreading centers. After accounting for these complications, the fracture zone appears capable of sustaining at least 20 MPa of shear stress and remains locked along the entire length of the fault except perhaps locally where it passed over the Tuamotu and Society hot spots

    Differential DNA methylation in blood as a mediator of the association between cigarette smoking and bladder cancer risk among postmenopausal women

    No full text
    Smoking accounts for approximately 52% of bladder cancer incidence among postmenopausal women, but the underlying mechanism is poorly understood. Our study investigates whether changes in DNA methylation, as measured in blood, mediate the impact of smoking on bladder cancer risk among postmenopausal women. We conducted analyses among 206 cases and 251 controls that were current or never smokers at baseline from a previous case-control study of bladder cancer and genome-wide DNA methylation nested within the Women’s Health Initiative. Separate mediation analyses were conducted for three CpG sites demonstrating robust associations with smoking in prior methylome-wide association studies: cg05575921 (AhRR), cg03636183 (F2RL3), and cg19859270 (GPR15). We estimated causal effects using the regression-based, four-way decomposition approach, which addresses the interaction between smoking and each CpG site. The overall proportion of the excess relative risk mediated by cg05575921 was 92% (p-value = 0.004) and by cg19859270 was 79% (p-value = 0.02). The largest component of the excess relative risk of bladder cancer due to 30 pack-years of smoking history in current smokers was the mediated interaction for both cg05575921 (72%, p = 0.02) and cg19859270 (72%, p-value = 0.04), where the mediated interaction is the effect of smoking on bladder cancer that both acts through differential methylation and depends on smoking history. There was little evidence that smoking was mediated through cg03636183. Our results suggest that differential methylation of cg05575921 and cg19859270 mediate the effects of smoking on bladder cancer, potentially revealing downstream effects of smoking relevant for carcinogenesis

    Nightshift work, chronotype, and genome-wide DNA methylation in blood

    No full text
    Molecular mechanisms underlying the negative health effects of shift work are poorly understood, which remains a barrier to developing intervention strategies to protect the long-term health of shift workers. We evaluated genome-wide differences in DNA methylation (measured in blood) between 111 actively employed female nightshift and 86 actively employed female dayshift workers from the Seattle metropolitan area. We also explored the effect of chronotype (i.e., measure of preference for activity earlier or later in the day) on DNA methylation among 110 of the female nightshift workers and an additional group of 131 male nightshift workers. Methylation data were generated using the Illumina Infinium HumanMethylation450 BeadChip (450K) Array. After applying the latest methylation data processing methods, we compared methylation levels at 361,210 CpG loci between the groups using linear regression models adjusted for potential confounders and applied the false-discovery rate (FDR) ≤ 0.05 to account for multiple comparisons. No statistically significant associations at the genome-wide level were observed with shift work or chronotype, though based on raw P values and absolute effect sizes, there were suggestive associations in genes that have been previously linked with cancer (e.g., BACH2, JRK, RPS6KA2) and type-2 diabetes (e.g., KCNQ1). Given that our study was underpowered to detect moderate effects, examining these suggestive results in well-powered independent studies or in pooled data sets may improve our understanding of the pathways underlying the negative health effects of shift work and the influence of personal factors such as chronotype. Such an approach may help identify potential interventions that can be used to protect the long-term health of shift workers
    corecore