Report on the May-June 2002 Englebright Lake deep coring campaign

This report describes the May-June 2002 Englebright Lake coring project. Englebright Lake is a 14-km-long reservoir on the Yuba River of northern California, impounded by Englebright Dam, which was completed in 1940. The sediments were cored to assess the current conditions in the reservoir as part of the California Bay-Delta Authority’s Upper Yuba River Studies Program. Sediment was collected using both hydraulic-piston and rotational coring equipment mounted on a floating drilling platform. Thirty boreholes were attempted at 7 sites spaced along the longitudinal axis of the reservoir. Complete sedimentary sections were recovered from 20 boreholes at 6 sites. In total, 335 m of sediment was cored, with 86% average recovery. The core sections (each up to 1.5 m long) were processed using a standard set of laboratory techniques, including geophysical logging of physical properties, splitting, visual descriptions, digital photography, and initial subsampling. This report presents the results of these analyses in a series of stratigraphic columns. Using the observed stratigraphy as a guide, several series of subsamples were collected for various sedimentologic, geochemical, and geochronological analyses. The results of laboratory analyses of most of these subsamples will be presented in future reports and articles

Shallow Rupture Propagation of Pleistocene Earthquakes Along the Hurricane Fault, UT, Revealed by Hematite (U-Th)/He Thermochronometry and Textures

The material properties and distribution of faults above the seismogenic zone promote or inhibit earthquake rupture propagation. We document the depths and mechanics of fault slip along the seismically active Hurricane fault, UT, with scanning and transmission electron microscopy and hematite (U-Th)/He thermochronometry. Hematite occurs as mm-scale, striated patches on a \u3e10 m2 thin, mirror-like silica fault surface. Hematite textures include bulbous aggregates and cataclasite, overlain by crystalline Fe-oxide nanorods and an amorphous silica layer at the slip interface. Textures reflect mechanical, fluid, and heat-assisted amorphization of hematite and silica-rich host rock that weaken the fault and promote rupture propagation. Hematite (U-Th)/He dates document episodes of mineralization and fault slip between 0.65 and 0.36 Ma at ∼300 m depth. Data illustrate that some earthquake ruptures repeatedly propagate along localized slip surfaces in the shallow crust and provide structural and material property constraints for in models of fault slip

Quantitative Chemically-Specific Coherent Diffractive Imaging of Buried Interfaces using a Tabletop EUV Nanoscope

Characterizing buried layers and interfaces is critical for a host of applications in nanoscience and nano-manufacturing. Here we demonstrate non-invasive, non-destructive imaging of buried interfaces using a tabletop, extreme ultraviolet (EUV), coherent diffractive imaging (CDI) nanoscope. Copper nanostructures inlaid in SiO2 are coated with 100 nm of aluminum, which is opaque to visible light and thick enough that neither optical microscopy nor atomic force microscopy can image the buried interfaces. Short wavelength (29 nm) high harmonic light can penetrate the aluminum layer, yielding high-contrast images of the buried structures. Moreover, differences in the absolute reflectivity of the interfaces before and after coating reveal the formation of interstitial diffusion and oxidation layers at the Al-Cu and Al-SiO2 boundaries. Finally, we show that EUV CDI provides a unique capability for quantitative, chemically-specific imaging of buried structures, and the material evolution that occurs at these buried interfaces, compared with all other approaches.Comment: 12 pages, 8 figure

Exploring Human/Animal Intersections: Converging Lines of Evidence in Comparative Models of Aging

At a symposium convened on March 8, 2007 by the Institute on Aging at the University of Pennsylvania, researchers from the University’s Schools of Medicine and Veterinary Medicine explored the convergence of aging research emerging from the two schools. Studies in human patients, animal models, and companion animals have revealed different but complementary aspects of the aging process, ranging from fundamental biologic aspects of aging to the treatment of age-related diseases, both experimentally and in clinical practice. Participants concluded that neither animal nor human research alone will provide answers to most questions about the aging process. Instead, an optimal translational research model supports a bidirectional flow of information from animal models to clinical research

TESS asteroseismology of the known red-giant host stars HD 212771 and HD 203949

International audienc

Delays in Leniency Application: Is There Really a Race to the Enforcer's Door?

This paper studies cartels’ strategic behavior in delaying leniency applications, a take-up decision that has been ignored in the previous literature. Using European Commission decisions issued over a 16-year span, we show, contrary to common beliefs and the existing literature, that conspirators often apply for leniency long after a cartel collapses. We estimate hazard and probit models to study the determinants of leniency-application delays. Statistical tests find that delays are symmetrically affected by antitrust policies and macroeconomic fluctuations. Our results shed light on the design of enforcement programs against cartels and other forms of conspiracy

Ernst Freund as Precursor of the Rational Study of Corporate Law

Gindis, David, Ernst Freund as Precursor of the Rational Study of Corporate Law (October 27, 2017). Journal of Institutional Economics, Forthcoming. Available at SSRN: https://ssrn.com/abstract=2905547, doi: https://dx.doi.org/10.2139/ssrn.2905547The rise of large business corporations in the late 19th century compelled many American observers to admit that the nature of the corporation had yet to be understood. Published in this context, Ernst Freund's little-known The Legal Nature of Corporations (1897) was an original attempt to come to terms with a new legal and economic reality. But it can also be described, to paraphrase Oliver Wendell Holmes, as the earliest example of the rational study of corporate law. The paper shows that Freund had the intuitions of an institutional economist, and engaged in what today would be called comparative institutional analysis. Remarkably, his argument that the corporate form secures property against insider defection and against outsiders anticipated recent work on entity shielding and capital lock-in, and can be read as an early contribution to what today would be called the theory of the firm.Peer reviewe

Loss of cardiomyocyte CYB5R3 impairs redox equilibrium and causes sudden cardiac death

Sudden cardiac death (SCD) in patients with heart failure (HF) is allied with an imbalance in reduction and oxidation (redox) signaling in cardiomyocytes; however, the basic pathways and mechanisms governing redox homeostasis in cardiomyocytes are not fully understood. Here, we show that cytochrome b5 reductase 3 (CYB5R3), an enzyme known to regulate redox signaling in erythrocytes and vascular cells, is essential for cardiomyocyte function. Using a conditional cardiomyocyte-specific CYB5R3-knockout mouse, we discovered that deletion of CYB5R3 in male, but not female, adult cardiomyocytes causes cardiac hypertrophy, bradycardia, and SCD. The increase in SCD in CYB5R3-KO mice is associated with calcium mishandling, ventricular fibrillation, and cardiomyocyte hypertrophy. Molecular studies reveal that CYB5R3-KO hearts display decreased adenosine triphosphate (ATP), increased oxidative stress, suppressed coenzyme Q levels, and hemoprotein dysregulation. Finally, from a translational perspective, we reveal that the high-frequency missense genetic variant rs1800457, which translates into a CYB5R3 T117S partial loss-of-function protein, associates with decreased event-free survival (~20%) in Black persons with HF with reduced ejection fraction (HFrEF). Together, these studies reveal a crucial role for CYB5R3 in cardiomyocyte redox biology and identify a genetic biomarker for persons of African ancestry that may potentially increase the risk of death from HFrEF.These studies were supported by NIH grants R35 HL 161177 (to ACS), R01 HL 133864 (to ACS), R01 HL 128304 (to ACS), R41 HL15098 (to GS), R01 GM 122091 (to PHT), GM125944 (to FJS), R01 DK112854 (to FJS), R21 NS112787 (to MF), NS121706 (to YLW), EB023507 (to YLW), F31 HL149241 (to HMS), and F31 HL151173 (to JCG). Support was also provided by American Heart Association grants 19EIA34770095 (to ACS), AHA 18CDA34140024 (to YLW), and 19PRE34380152 (to NTC); the Spanish Ministry of Health (grant FIS PI17-01286); Junta de Andalucía BIO-177 and the FEDER Funding Program from the European Union and CIBERER (U729)-ISCIII (to PN); Department of Defense W81XWH1810070 (to YLW); and Vitalant. This research was supported in part by the University of Pittsburgh Center for Research Computing through the resources provided. Specifically, this work used the HTC cluster, which is supported by NIH award number S10OD028483.Peer reviewe

Fetal Demise and Failed Antibody Therapy During Zika Virus Infection of Pregnant Macaques

Zika virus (ZIKV) infection of pregnant women is associated with pathologic complications of fetal development. Here, we infect pregnant rhesus macaques (Macaca mulatta) with a minimally passaged ZIKV isolate from Rio de Janeiro, where a high rate of fetal development complications was observed. The infection of pregnant macaques with this virus results in maternal viremia, virus crossing into the amniotic fluid (AF), and in utero fetal deaths. We also treated three additional ZIKV-infected pregnant macaques with a cocktail of ZIKV-neutralizing human monoclonal antibodies (nmAbs) at peak viremia. While the nmAbs can be effective in clearing the virus from the maternal sera of treated monkeys, it is not sufficient to clear ZIKV from AF. Our report suggests that ZIKV from Brazil causes fetal demise in non-human primates (NHPs) without additional mutations or confounding co-factors. Treatment with a neutralizing anti-ZIKV nmAb cocktail is insufficient to fully stop vertical transmission

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition