Tsunami waveform analyses of the 2006 underthrust and 2007 outer-rise Kurile earthquakes

International audienceThe 2006 large interplate Kurile earthquake proved that the entire plate interface of the Kurile-Kamchatka subduction zone was strongly coupled from Hokkaido, Japan, to Kamchatka, Russia. The seismic moment of the 2006 Kurile earthquake estimated from ten tsunami waveforms is 3.1×1021 Nm (Mw=8.3). This estimate is consistent with the seismic moment estimated from the seismological data in the Global CMT catalog. The computed tsunami propagation indicates that scattering of the tsunami waves occurred at the shallow region near the Emperor Ridge. The computed tsunami propagation also indicates that large later tsunami waves observed at Crescent City is caused by the shallow region along the Mendocino Fracture Zone. The seismic moment of the 2007 outer-rise Kurile earthquake estimated from tsunami waveforms is 1.0×1021 Nm (Mw=8.0). This estimate is also consistent with the seismic moment in the Global CMT catalog

Pressure-induced reconstitution of Fermi surfaces and spin fluctuations in S-substituted FeSe

FeSe is a unique high-Tc iron-based superconductor in which nematicity, superconductivity, and magnetism are entangled with each other in the P-T phase diagram. We performed ⁷⁷Se-nuclear magnetic resonance measurements under pressures of up to 3.9 GPa on 12% S-substituted FeSe, in which the complex overlap between the nematicity and magnetism are resolved. A pressure-induced Lifshitz transition was observed at 1.0 GPa as an anomaly of the density of states and as double superconducting (SC) domes accompanied by different types of antiferromagnetic (AF) fluctuations. The low-Tc SC dome below 1 GPa is accompanied by strong AF fluctuations, whereas the high-Tc SC dome develops above 1 GPa, where AF fluctuations are fairly weak. These results suggest the importance of the dxy orbital and its intra-orbital coupling for the high-Tc superconductivity

Identification of the protein kinases Pyk3 and Phg2 as regulators of the STATc-mediated response to hyperosmolarity

Cellular adaptation to changes in environmental osmolarity is crucial for cell survival. In Dictyostelium, STATc is a key regulator of the transcriptional response to hyperosmotic stress. Its phosphorylation and consequent activation is controlled by two signaling branches, one cGMP- and the other Ca(2+)-dependent, of which many signaling components have yet to be identified. The STATc stress signalling pathway feeds back on itself by upregulating the expression of STATc and STATc-regulated genes. Based on microarray studies we chose two tyrosine-kinase like proteins, Pyk3 and Phg2, as possible modulators of STATc phosphorylation and generated single and double knock-out mutants to them. Transcriptional regulation of STATc and STATc dependent genes was disturbed in pyk3(-), phg2(-), and pyk3(-)/phg2(-) cells. The absence of Pyk3 and/or Phg2 resulted in diminished or completely abolished increased transcription of STATc dependent genes in response to sorbitol, 8-Br-cGMP and the Ca(2+) liberator BHQ. Also, phospho-STATc levels were significantly reduced in pyk3(-) and phg2(-) cells and even further decreased in pyk3(-)/phg2(-) cells. The reduced phosphorylation was mirrored by a significant delay in nuclear translocation of GFP-STATc. The protein tyrosine phosphatase 3 (PTP3), which dephosphorylates and inhibits STATc, is inhibited by stress-induced phosphorylation on S448 and S747. Use of phosphoserine specific antibodies showed that Phg2 but not Pyk3 is involved in the phosphorylation of PTP3 on S747. In pull-down assays Phg2 and PTP3 interact directly, suggesting that Phg2 phosphorylates PTP3 on S747 in vivo. Phosphorylation of S448 was unchanged in phg2(-) cells. We show that Phg2 and an, as yet unknown, S448 protein kinase are responsible for PTP3 phosphorylation and hence its inhibition, and that Pyk3 is involved in the regulation of STATc by either directly or indirectly activating it. Our results add further complexities to the regulation of STATc, which presumably ensure its optimal activation in response to different environmental cues

Differentiation-Inducing Factor-1 and -2 Function also as Modulators for Dictyostelium Chemotaxis

BackgroundIn the early stages of development of the cellular slime mold Dictyostelium discoideum, chemotaxis toward cAMP plays a pivotal role in organizing discrete cells into a multicellular structure. In this process, a series of signaling molecules, such as G-protein-coupled cell surface receptors for cAMP, phosphatidylinositol metabolites, and cyclic nucleotides, function as the signal transducers for controlling dynamics of cytoskeleton. Differentiation-inducing factor-1 and -2 (DIF-1 and DIF-2) were originally identified as the factors (chlorinated alkylphenones) that induce Dictyostelium stalk cell differentiation, but it remained unknown whether the DIFs had any other physiologic functions.Methodology/Principal FindingsTo further elucidate the functions of DIFs, in the present study we investigated their effects on chemotaxis under various conditions. Quite interestingly, in shallow cAMP gradients, DIF-1 suppressed chemotaxis whereas DIF-2 promoted it greatly. Analyses with various mutants revealed that DIF-1 may inhibit chemotaxis, at least in part, via GbpB (a phosphodiesterase) and a decrease in the intracellular cGMP concentration ([cGMP]i). DIF-2, by contrast, may enhance chemotaxis, at least in part, via RegA (another phosphodiesterase) and an increase in [cGMP]i. Using null mutants for DimA and DimB, the transcription factors that are required for DIF-dependent prestalk differentiation, we also showed that the mechanisms for the modulation of chemotaxis by DIFs differ from those for the induction of cell differentiation by DIFs, at least in part.Conclusions/SignificanceOur findings indicate that DIF-1 and DIF-2 function as negative and positive modulators for Dictyostelium chemotaxis, respectively. To our knowledge, this is the first report in any organism of physiologic modulators (small molecules) for chemotaxis having differentiation-inducing activity

Real-Time Black Carbon Emission Factor Measurements from Light Duty Vehicles

Eight light-duty gasoline low emission vehicles (LEV I) were tested on a Chassis dynamometer using the California Unified Cycle (UC) at the Haagen-Smit vehicle test facility at the California Air Resources Board in El Monte, CA during September 2011. The UC includes a cold start phase followed by a hot stabilized running phase. In addition, a light-duty gasoline LEV vehicle and ultralow emission vehicle (ULEV), and a light-duty diesel passenger vehicle and gasoline direct injection (GDI) vehicle were tested on a constant velocity driving cycle. A variety of instruments with response times ≥0.1 Hz were used to characterize how the emissions of the major particulate matter components varied for the LEVs during a typical driving cycle. This study focuses primarily on emissions of black carbon (BC). These measurements allowed for the determination of BC emission factors throughout the driving cycle, providing insights into the temporal variability of BC emission factors during different phases of a typical driving cycle

MEDICAL TREATMENT OF UNRUPTURED CEREBRAL ANEURYSMS

Background: Currently there are no pharmacological therapies for patients with unruptured cerebral aneurysms. Elsewhere we showed that the mineralocorticoid receptor antagonist eplerenone prevented the formation of cerebral aneurysms in our ovariectomized hypertensive aneurysm rat model. The current pilot study evaluated whether it can be used to prevent the growth and rupture of cerebral aneurysms in hypertensive patients. Methods: Between August 2011 and May 2014, we enrolled 82 patients with 90 aneurysms in an open-label uncontrolled clinical trial. All provided prior informed consent for inclusion in this study, and all were treated with eplerenone (25-100 mg/d). The primary end points of our study were the rupture and enlargement of the cerebral aneurysms. Results: Of the 82 patients, 80 (88 unruptured aneurysms) were followed for a mean of 21.3 months (153.4 aneurysm-years); 12 patients (15.0%) permanently discontinued taking the drug. One month after the start of eplerenone administration and throughout the follow-up period, eplerenone kept the blood pressure within the normal range. Most notably, no aneurysms smaller than 9 mm ruptured or enlarged. However, of 2 large thrombosed aneurysms, 1 enlarged and the other ruptured. The overall annual rupture rate was .65%; it was 13.16% for aneurysms larger than 10 mm; the overall annual rate for reaching the primary end points was 1.30%. Conclusion: Our observations suggest that eplerenone may help to prevent the growth and rupture of unruptured cerebral aneurysms smaller than 9 mm. To assess its potential long-term clinical benefits, large clinical trials are needed

Ultra-Rapid Warming Yields High Survival of Mouse Oocytes Cooled to −196°C in Dilutions of a Standard Vitrification Solution

Intracellular ice is generally lethal. One way to avoid it is to vitrify cells; that is, to convert cell water to a glass rather than to ice. The belief has been that this requires both the cooling rate and the concentration of glass-inducing solutes be very high. But high solute concentrations can themselves be damaging. However, the findings we report here on the vitrification of mouse oocytes are not in accord with the first belief that cooling needs to be extremely rapid. The important requirement is that the warming rate be extremely high. We subjected mouse oocytes in the vitrification solution EAFS 10/10 to vitrification procedures using a broad range of cooling and warming rates. Morphological survivals exceeded 80% when they were warmed at the highest rate (117,000°C/min) even when the prior cooling rate was as low as 880°C/min. Functional survival was >81% and 54% with the highest warming rate after cooling at 69,000 and 880°C/min, respectively. Our findings are also contrary to the second belief. We show that a high percentage of mouse oocytes survive vitrification in media that contain only half the usual concentration of solutes, provided they are warmed extremely rapidly; that is, >100,000°C/min. Again, the cooling rate is of less consequence

The California baseline ozone transport study (CABOTS)

Ozone is one of the six criteria pollutants identified by the U.S. Clean Air Act Amendment of 1970 as particularly harmful to human health. Concentrations have decreased markedly across the United States over the past 50 years in response to regulatory efforts, but continuing research on its deleterious effects have spurred further reductions in the legal threshold. The South Coast and San Joaquin Valley Air Basins of California remain the only two extreme ozone nonattainment areas in the United States. Further reductions of ozone in the West are complicated by significant background concentrations whose relative importance increases as domestic anthropogenic contributions decline and the national standards continue to be lowered. These background concentrations derive largely from uncontrollable sources including stratospheric intrusions, wildfires, and intercontinental transport. Taken together the exogenous sources complicate regulatory strategies and necessitate a much more precise understanding of the timing and magnitude of their contributions to regional air pollution. The California Baseline Ozone Transport Study was a field campaign coordinated across Northern and Central California during spring and summer 2016 aimed at observing daily variations in the ozone columns crossing the North American coastline, as well as the modification of the ozone layering downwind across the mountainous topography of California to better understand the impacts of background ozone on surface air quality in complex terrain

Two <em>Dictyostelium</em> Tyrosine Kinase-Like kinases function in parallel, stress-induced STAT activation pathways

When Dictyostelium cells are hyperosmotically stressed, STATc is activated by tyrosine phosphorylation. Unusually, activation is regulated by serine phosphorylation and consequent inhibition of a tyrosine phosphatase: PTP3. The identity of the cognate tyrosine kinase is unknown, and we show that two tyrosine kinase–like (TKL) enzymes, Pyk2 and Pyk3, share this function; thus, for stress-induced STATc activation, single null mutants are only marginally impaired, but the double mutant is nonactivatable. When cells are stressed, Pyk2 and Pyk3 undergo increased autocatalytic tyrosine phosphorylation. The site(s) that are generated bind the SH2 domain of STATc, and then STATc becomes the target of further kinase action. The signaling pathways that activate Pyk2 and Pyk3 are only partially overlapping, and there may be a structural basis for this difference because Pyk3 contains both a TKL domain and a pseudokinase domain. The latter functions, like the JH2 domain of metazoan JAKs, as a negative regulator of the kinase domain. The fact that two differently regulated kinases catalyze the same phosphorylation event may facilitate specific targeting because under stress, Pyk3 and Pyk2 accumulate in different parts of the cell; Pyk3 moves from the cytosol to the cortex, whereas Pyk2 accumulates in cytosolic granules that colocalize with PTP3