1,358 research outputs found

    Should Society Punish or Reform the Criminal?

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    Millimeter-level precision in a seafloor geodesy experiment at the Discovery transform fault, East Pacific Rise

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    Author Posting. Ā© American Geophysical Union, 2013. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geochemistry, Geophysics, Geosystems 14 (2013): 4392ā€“4402, doi:10.1002/ggge.20225.Direct-path acoustic ranging is a promising seafloor geodetic technique for continuous high-resolution monitoring of geodynamical process such as fault slip and magma intrusion. Here we report on a yearlong acoustic ranging experiment conducted across the discovery transform fault at āˆ¼4Ā°S on the East Pacific Rise. The ranging instruments utilized a novel acoustic signal designed to enhance precision. We find that, after correcting for variations in sound speed at the path end-points, the ranging measurements have a precision of āˆ¼1 mm over baselines approaching 1 km in length. The primary difficulty in this particular experiment was with the physical stability of the benchmarks, which were deployed free fall from a ship. Despite the stability issues, it appears that the portion of the transform fault that the array covered was locked during the year of our survey. The primary obstacle to continuous, high sample rate, high-precision geodetic monitoring of oceanic ridges and transform faults is now limited to the construction of geodetic monuments that are well anchored into bedrock.This research was funded by the National Science Foundation OCE division under award 0351143.2014-04-0

    Characterization and Functions of Protease-Activated Receptor 2 in Obesity, Diabetes, and Metabolic Syndrome: A Systematic Review

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    Proteinase-activated receptor 2 (PAR2) is a cell surface receptor activated by serine proteinases or specific synthetic compounds. Interest in PAR2 as a pharmaceutical target for various diseases is increasing. Here we asked two questions relevant to endothelial dysfunction and diabetes: How is PAR2 function affected in blood vessels? What role does PAR2 have in promoting obesity, diabetes, and/or metabolic syndrome, specifically via the endothelium and adipose tissues? We conducted a systematic review of the published literature in PubMed and Scopus (July 2015; search terms: par2, par-2, f2lr1, adipose, obesity, diabetes, and metabolic syndrome). Seven studies focused on PAR2 and vascular function. The obesity, diabetes, or metabolic syndrome animal models differed amongst studies, but each reported that PAR2-mediated vasodilator actions were preserved in the face of endothelial dysfunction. The remaining studies focused on nonvascular functions and provided evidence supporting the concept that PAR2 activation promoted obesity. Key studies showed that PAR2 activation regulated cellular metabolism, and PAR2 antagonists inhibited adipose gain and metabolic dysfunction in rats.We conclude that PAR2 antagonists for treatment of obesity indeed show early promise as a therapeutic strategy; however, endothelial-specific PAR2 functions, which may offset mechanisms that produce vascular dysfunction in diabetes, warrant additional study

    Dynamic triggering and earthquake swarms on East Pacific Rise transform faults

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    Author Posting. Ā© American Geophysical Union, 2017. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geophysical Research Letters 44 (2017): 702-710, doi:10.1002/2016GL070857.While dynamic earthquake triggering has been reported in several continental settings, offshore observations are rare. Oceanic transform faults share properties with continental geothermal areas known for dynamic triggering: high geothermal gradients, high seismicity rates, and frequent swarms. We study dynamic triggering along the East Pacific Rise by analyzing 1 year of seismicity recorded by Ocean Bottom Seismographs. By comparing the response to teleseismic waves from global earthquakes, we find triggering to be most sensitive to changes in normal stress and to preferentially occur above 0.25 kPa. The clearest example of triggering occurs on the Quebrada and Gofar faults after the Mw8.0 Wenchuan earthquake. On Gofar, triggered seismicity occurs between the rupture areas of large earthquakes, within a zone characterized by aseismic slip, abundant microseismicity, frequent swarms, and low Vp. We infer that lithological properties inhibiting rupture propagation, such as high porosity and fluid content, also favor dynamic triggering.WHOI SSF program; GeoSim Career Support fellowship; USGS Grant Number: G14AP000582017-07-1

    Blood pressures, heart rate and locomotor activity during salt loading and angiotensin II infusion in protease-activated receptor 2 (PAR2) knockout mice

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    <p>Abstract</p> <p>Background</p> <p>In this study we used radiotelemetry to measure hemodynamic variables and locomotor activity in conscious unrestrained male Protease-Activated Receptor 2 (PAR-2) knockout mice in order to provide a detailed assessment of their blood pressure phenotype. In addition we tested for an influence of PAR-2 on salt-sensitivity (8% versus 0.5% NaCl diet, 2.5 weeks) and angiotensin II-induced hypertension (1 Ī¼g Ile<sup>5</sup>-angiotensin II/kg/min versus 0.25 Ī¼l/h saline, 2 weeks).</p> <p>Results</p> <p>Systolic arterial pressures of PAR-2 -/- (129 Ā± 1 mmHg, n = 21, P < 0.05) were statistically higher than those of C57BL/6J (124 Ā± 1 mmHg, n = 33) throughout the 24 h period under baseline conditions. Pulse pressures in PAR-2 -/- were also significantly elevated (33 Ā± 1 mmHg versus 30 Ā± 1 mmHg, P < 0.05), whereas diastolic arterial pressures were not. Heart rates in PAR-2 -/- were not significantly different than controls, with the exception that heart rate of PAR-2 -/- was 23 beats per min higher than controls (<it>P </it>< 0.001) during periods of nocturnal activity. The diurnal pattern and intensity of locomotor activity were not found to differ between strains. A high salt diet led to increased blood pressures, decreased heart rates, increased time spent active and decreased intensity levels of locomotor activity. Salt-induced changes in systolic and pulse pressures in PAR-2 -/- were less than in C57B/6J. Angiotensin II treatment increased pressures, decreased heart rates, decreased time spent active and decreased intensity levels of activity of PAR-2 -/-, all to the same extent as C57BL/6J. A trend of lower blood pressures during the middle period of angiotensin II treatment period was observed in individual PAR-2 -/-.</p> <p>Conclusion</p> <p>The data indicated gene knockout of PAR-2 was associated with a modest change in blood pressure phenotype. PAR-2 -/- mice exhibited moderate elevation of systolic arterial and pulse pressures, yet no increased diastolic arterial pressure, no increased blood pressure responses to high salt diet and a subtle difference in the time course of the blood pressure responses to angiotensin II infusion.</p

    Comparative genomic analysis reveals a novel mitochondrial isoform of human rTS protein and unusual phylogenetic distribution of the rTS gene

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    BACKGROUND: The rTS gene (ENOSF1), first identified in Homo sapiens as a gene complementary to the thymidylate synthase (TYMS) mRNA, is known to encode two protein isoforms, rTSĪ± and rTSĪ². The rTSĪ² isoform appears to be an enzyme responsible for the synthesis of signaling molecules involved in the down-regulation of thymidylate synthase, but the exact cellular functions of rTS genes are largely unknown. RESULTS: Through comparative genomic sequence analysis, we predicted the existence of a novel protein isoform, rTS, which has a 27 residue longer N-terminus by virtue of utilizing an alternative start codon located upstream of the start codon in rTSĪ². We observed that a similar extended N-terminus could be predicted in all rTS genes for which genomic sequences are available and the extended regions are conserved from bacteria to human. Therefore, we reasoned that the protein with the extended N-terminus might represent an ancestral form of the rTS protein. Sequence analysis strongly predicts a mitochondrial signal sequence in the extended N-terminal of human rTSĪ³, which is absent in rTSĪ². We confirmed the existence of rTS in human mitochondria experimentally by demonstrating the presence of both rTSĪ³ and rTSĪ² proteins in mitochondria isolated by subcellular fractionation. In addition, our comprehensive analysis of rTS orthologous sequences reveals an unusual phylogenetic distribution of this gene, which suggests the occurrence of one or more horizontal gene transfer events. CONCLUSION: The presence of two rTS isoforms in mitochondria suggests that the rTS signaling pathway may be active within mitochondria. Our report also presents an example of identifying novel protein isoforms and for improving gene annotation through comparative genomic analysis

    A lack of dynamic triggering of slow slip and tremor indicates that the shallow Cascadia megathrust offshore Vancouver Island is likely locked

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    Author Posting. Ā© American Geophysical Union, 2018. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geophysical Research Letters 45 (2018): 11,095-11,103, doi:10.1029/2018GL079519.Great subduction zone earthquakes vary considerably in the updip extent of megathrust rupture. It is unclear if this diversity reflects variations in interseismic strain accumulation owing to the limited number of subduction zones with seafloor monitoring. We use a borehole seismicā€geodetic observatory installed at the updip end of the Cascadia fault offshore Vancouver Island to show that the megathrust there does not appear to slip in triggered tremor or slowā€slip events when subjected to moderate dynamic stress transients. Borehole tilt and seismic data from recent teleseismic M7.6ā€“8.1 earthquakes demonstrate a lack of triggered slow slip above the Mw 4.0 level and an absence of triggered tremor despite shearā€stress transients of 1ā€“10 kPa that were sufficient to trigger tremor on the downdip end of the interface. Our observations are most consistent with a model in which the Cascadia fault offshore Vancouver Island is locked all the way to the trench.NSF Grant Numbers: OCEā€1259243, OCEā€1259718; W. M. Keck Foundation2019-04-2

    Spatial and temporal variations in earthquake stress drop on Gofar Transform Fault, East Pacific Rise : implications for fault strength

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    Author Posting. Ā© American Geophysical Union, 2018. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research: Solid Earth 123 (2018): 7722-7740, doi:10.1029/2018JB015942.On Gofar Transform Fault on the East Pacific Rise, the largest earthquakes (6.0 ā‰¤ MW ā‰¤ 6.2) have repeatedly ruptured the same portion of the fault, while intervening fault segments host swarms of microearthquakes. These longā€term patterns in earthquake occurrence suggest that heterogeneous fault zone properties control earthquake behavior. Using waveforms from ocean bottom seismometers that recorded seismicity before and after an anticipated 2008 MW 6.0 mainshock, we investigate the role that differences in material properties have on earthquake rupture at Gofar. We determine stress drop for 138 earthquakes (2.3 ā‰¤ MW ā‰¤ 4.0) that occurred within and between the rupture areas of large earthquakes. Stress drops are calculated from corner frequencies derived using an empirical Green's function spectral ratio method, and seismic moments are obtained by fitting the omegaā€square source model to the low frequency amplitude of the displacement spectrum. Our analysis yields stress drops from 0.04 to 3.2 MPa with statistically significant spatial variation, including ~2 times higher average stress drop in fault segments where large earthquakes also occur compared to fault segments that host earthquake swarms. We find an inverse correlation between stress drop and P wave velocity reduction, which we interpret as the effect of fault zone damage on the ability of the fault to store strain energy that leads to our spatial variations in stress drop. Additionally, we observe lower stress drops following the MW 6.0 mainshock, consistent with increased damage and decreased fault strength after a large earthquake.W. M. Keck Foundation; National Science Foundation Division of Ocean Sciences (OCE) Grant Number: 13525652019-03-0

    Observations of seismicity and ground motion in the Northeast U.S. Atlantic Margin from oceanā€bottom seismometer data

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    Author Posting. Ā© Seismological Society of America, 2016. This article is posted here by permission of Seismological Society of America for personal use, not for redistribution. The definitive version was published in Seismological Research Letters 88 (2017): 23-31, doi:10.1785/0220160079.Earthquake data from two shortā€period oceanā€bottom seismometer (OBS) networks deployed for over a year on the continental slope off New York and southern New England were used to evaluate seismicity and ground motions along the continental margin. Our OBS networks located only one earthquake of Mcāˆ¼1.5 near the shelf edge during six months of recording, suggesting that seismic activity (MLg>3.0) of the margin as far as 150ā€“200 km offshore is probably successfully monitored by land stations without the need for OBS deployments. The spectral acceleration from two local earthquakes recorded by the OBS was found to be generally similar to the acceleration from these earthquakes recorded at several seismic stations on land and to hybrid empirical acceleration relationships for eastern North America. Therefore, the seismic attenuation used for eastern North America can be extended in this region at least to the continental slope. However, additional offshore studies are needed to verify these preliminary conclusions.This project was partially funded by the Nuclear Regulatory Commission under NRC Job Number V6166.2017-11-0
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