29 research outputs found

    Study on Coulomb Stress Triggering of the April 2015 M7.8 Nepal Earthquake Sequence

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    In April 2015, a M7.8 earthquake occurred less than one month before a M7.3 earthquake near Kodari, Nepal. The Nepal earthquake sequences also include four larger (M > 6) aftershocks. To reveal the interrelation between the main shock and the aftershocks, we check the role of coseismic coulomb stress triggering on aftershocks that follow the M7.8 main shock. Based on the focal mechanisms of the aftershocks and source models of the main shock, the coulomb failure stress changes on both of the focal mechanism nodal planes are calculated. In addition, the coulomb stress changes on the focal sources of each aftershock are also calculated. A large proportion of the M > 6 aftershocks occurred in positive coulomb stress areas triggered by the M7.8 main shock. The secondary triggering effect of the M7.3 aftershock is also found in this paper. More specifically, the M7.3 aftershock promoted failure on the rupture plane of the M6.3 aftershock. Therefore, we may conclude that the majority of larger aftershocks, which accumulated positive coulomb stress changes during the sequence, were promoted or triggered by the main shock failure. It suggests that coulomb stress triggering contributed to the evolution of the Nepal M7.8 earthquake sequence

    Transcription factor Hlx controls a systematic switch from white to brown fat through Prdm16-mediated co-activation

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    Browning of subcutaneous white fat (iWAT) involves several reprograming events, but the underlying mechanisms are incompletely understood. Here we show that the transcription factor Hlx is selectively expressed in brown adipose tissue (BAT) and iWAT, and is translationally upregulated by beta3-adrenergic signaling-mediated suppression of the translational inhibitor 4E-BP1. Hlx interacts with and is co-activated by Prdm16 to control BAT-selective gene expression and mitochondrial biogenesis. Hlx heterozygous knockout mice have defects in brown-like adipocyte formation in iWAT, and develop glucose intolerance and high fat-induced hepatic steatosis. Conversely, transgenic expression of Hlx at a physiological level drives a full program of thermogenesis and converts iWAT to brown-like fat, which improves glucose homeostasis and prevents obesity and hepatic steatosis. The adipose remodeling phenotypes are recapitulated by fat-specific injection of Hlx knockdown and overexpression viruses, respectively. Our studies establish Hlx as a powerful regulator for systematic white adipose tissue browning and offer molecular insights into the underlying transcriptional mechanism.The transcriptional co-activator Prdm16 regulates browning of white adipose tissue (WAT). Here, the authors show that Prdm16 interacts with the transcription factor Hlx, which is stabilized in response to beta3-adrenergic signaling, to increase thermogenic gene expression and mitochondrial biogenesis in subcutaneous WAT

    Jmjd3-Mediated H3K27me3 Dynamics Orchestrate Brown Fat Development and Regulate White Fat Plasticity

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    SummaryProgression from brown preadipocytes to adipocytes engages two transcriptional programs: the expression of adipogenic genes common to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective genes. However, the dynamics of chromatin states and epigenetic enzymes involved remain poorly understood. Here we show that BAT development is selectively marked and guided by repressive H3K27me3 and is executed by its demethylase Jmjd3. We find that a significant subset of BAT-selective genes, but not common fat genes or WAT-selective genes, are demarcated by H3K27me3 in both brown and white preadipocytes. Jmjd3-catalyzed removal of H3K27me3, in part through Rreb1-mediated recruitment, is required for expression of BAT-selective genes and for development of beige adipocytes both in vitro and in vivo. Moreover, gain- and loss-of-function Jmjd3 transgenic mice show age-dependent body weight reduction and cold intolerance, respectively. Together, we identify an epigenetic mechanism governing BAT fate determination and WAT plasticity

    Capacity of Gaussian Channels With Duty Cycle and Power Constraints

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    Study on Coulomb Stress Triggering of the April 2015 M7.8 Nepal Earthquake Sequence

    Get PDF
    In April 2015, a M7.8 earthquake occurred less than one month before a M7.3 earthquake near Kodari, Nepal. The Nepal earthquake sequences also include four larger (M > 6) aftershocks. To reveal the interrelation between the main shock and the aftershocks, we check the role of coseismic coulomb stress triggering on aftershocks that follow the M7.8 main shock. Based on the focal mechanisms of the aftershocks and source models of the main shock, the coulomb failure stress changes on both of the focal mechanism nodal planes are calculated. In addition, the coulomb stress changes on the focal sources of each aftershock are also calculated. A large proportion of the M > 6 aftershocks occurred in positive coulomb stress areas triggered by the M7.8 main shock. The secondary triggering effect of the M7.3 aftershock is also found in this paper. More specifically, the M7.3 aftershock promoted failure on the rupture plane of the M6.3 aftershock. Therefore, we may conclude that the majority of larger aftershocks, which accumulated positive coulomb stress changes during the sequence, were promoted or triggered by the main shock failure. It suggests that coulomb stress triggering contributed to the evolution of the Nepal M7.8 earthquake sequence

    Baseline correction for digital strong-motion records by using the pre-event portion

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    Baseline offset in digital strong-motion acceleration record and initial velocity can produce unrealistic results for ground velocity and displacement derived from the acceleration by integration. A new method is proposed for the baseline correction and initial velocity calculation. It is based on linear least-squares fitting of the pre-event portion of velocity derived from the uncorrected acceleration data. Compared with the conventional method, which is based on removing the mean values of the pre-event portions of the acceleration and velocity traces, this method has clearer physical meaning and better stability
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