844 research outputs found

    Patterns of depredation in the Hawai‘i deep-set longline fishery informed by fishery and false killer whale behavior

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    False killer whales (Pseudorca crassidens) depredate bait and catch in the Hawai‘i-based deep-set longline fishery, and as a result, this species is hooked or entangled more than any other cetacean in this fishery. We analyzed data collected by fisheries observers and from satellite-linked transmitters deployed on false killer whales to identify patterns of odontocete depredation that could help fishermen avoid overlap with whales. Odontocete depredation was observed on ˜6% of deep-set hauls across the fleet from 2004 to 2018. Model outcomes from binomial GAMMs suggested coarse patterns, for example, higher rates of depredation in winter, at lower latitudes, and with higher fishing effort. However, explanatory power was low, and no covariates were identified that could be used in a predictive context. The best indicator of depredation was the occurrence of depredation on a previous set of the same vessel. We identified spatiotemporal scales of this repeat depredation to provide guidance to fishermen on how far to move or how long to wait to reduce the probability of repeated interactions. The risk of depredation decreased with both space and time from a previous occurrence, with the greatest benefits achieved by moving ˜400 km or waiting ˜9 d, which reduced the occurrence of depredation from 18% to 9% (a 50% reduction). Fishermen moved a median 46 km and waited 4.7 h following an observed depredation interaction, which our analysis suggests is unlikely to lead to large reductions in risk. Satellite-tagged pelagic false killer whales moved up to 75 km in 4 h and 335 km in 24 h, suggesting that they can likely keep pace with longline vessels for at least four hours and likely longer. We recommend fishermen avoid areas of known depredation or bycatch by moving as far and as quickly as practical, especially within a day or two of the depredation or bycatch event. We also encourage captains to communicate depredation and bycatch occurrence to enable other vessels to similarly avoid high-risk areas

    Upper mantle seismic anisotropy at a strike-slip boundary: South Island, New Zealand

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    New shear wave splitting measurements made from stations onshore and offshore the South Island of New Zealand show a zone of anisotropy 100–200 km wide. Measurements in central South Island and up to approximately 100 km offshore from the west coast yield orientations of the fast quasi-shear wave nearly parallel to relative plate motion, with increased obliquity to this orientation observed farther from shore. On the eastern side of the island, fast orientations rotate counterclockwise to become nearly perpendicular to the orientation of relative plate motion approximately 200 km off the east coast. Uniform delay times between the fast and slow quasi-shear waves of nearly 2.0 s onshore continue to stations approximately 100 km off the west coast, after which they decrease to ~1 s at 200 km. Stations more than ~300 km from the west coast show little to no splitting. East coast stations have delay times around 1 s. Simple strain fields calculated from a thin viscous sheet model (representing distributed lithospheric deformation) with strain rates decreasing exponentially to both the northwest and southeast with e-folding dimensions of 25–35 km (approximately 75% of the deformation within a zone 100–140 km wide) match orientations and amounts of observed splitting. A model of deformation localized in the lithosphere and then spreading out in the asthenosphere also yields predictions consistent with observed splitting if, at depths of 100–130 km below the lithosphere, typical grain sizes are ~ 6–7 mm.New Zealand. Ministry of Research, Science, and TechnologyNational Science Foundation (U.S.). Continental Dynamics Program (Grant EAR-0409564)National Science Foundation (U.S.). Continental Dynamics Program (Grant EAR-0409609)National Science Foundation (U.S.). Continental Dynamics Program (Grant EAR-0409835

    Proteomic analysis of plasma membrane and secretory vesicles from human neutrophils

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    <p>Abstract</p> <p>Background</p> <p>Polymorphonuclear neutrophils (PMN) constitute an essential cellular component of innate host defense against microbial invasion and exhibit a wide array of responses both to particulate and soluble stimuli. As the cells recruited earliest during acute inflammation, PMN respond rapidly and release a variety of potent cytotoxic agents within minutes of exposure to microbes or their products. PMN rely on the redistribution of functionally important proteins, from intracellular compartments to the plasma membrane and phagosome, as the means by which to respond quickly. To determine the range of membrane proteins available for rapid recruitment during PMN activation, we analyzed the proteins in subcellular fractions enriched for plasma membrane and secretory vesicles recovered from the light membrane fraction of resting PMN after Percoll gradient centrifugation and free-flow electrophoresis purification using mass spectrometry-based proteomics methods.</p> <p>Results</p> <p>To identify the proteins light membrane fractions enriched for plasma membrane vesicles and secretory vesicles, we employed a proteomic approach, first using MALDI-TOF (peptide mass fingerprinting) and then by HPLC-MS/MS using a 3D ion trap mass spectrometer to analyze the two vesicle populations from resting PMN. We identified several proteins that are functionally important but had not previously been recovered in PMN secretory vesicles. Two such proteins, 5-lipoxygenase-activating protein (FLAP) and dysferlin were further validated by immunoblot analysis.</p> <p>Conclusion</p> <p>Our data demonstrate the broad array of proteins present in secretory vesicles that provides the PMN with the capacity for remarkable and rapid reorganization of its plasma membrane after exposure to proinflammatory agents or stimuli.</p

    Why have asset price properties changed so little in 200 years

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    We first review empirical evidence that asset prices have had episodes of large fluctuations and been inefficient for at least 200 years. We briefly review recent theoretical results as well as the neurological basis of trend following and finally argue that these asset price properties can be attributed to two fundamental mechanisms that have not changed for many centuries: an innate preference for trend following and the collective tendency to exploit as much as possible detectable price arbitrage, which leads to destabilizing feedback loops.Comment: 16 pages, 4 figure

    Sarcopenia is a Significant Predictor of Mortality After Abdominal Aortic Aneurysm Repair

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    Aims Repair of abdominal aortic aneurysms (AAA) decreases the incidence of rupture and death. In cancer patients, sarcopenia has been associated with increased surgical complications and mortality. The impact of sarcopenia on survival after AAA repair has yet to be described. Methods and Results Patient demographic, laboratory, body composition measurements and survival data were obtained from patients undergoing AAA repair at the Indiana University medical campus over a 5-year period. Univariate and multivariate analyses were performed to identify factors associated with overall survival. Overall, 58.2% presented with sarcopenia. Sarcopenic patients were older (71.8±8.3 versus 66.8±8.1 years; p<0.001), had lower body mass index (BMI) (26.3±5.2 versus 31.5±5.9 kg/m2; p<0.001), higher rates of myosteatosis (84.4% versus 52.%; p<0.001), greater AAA diameter (60.6±14.0 versus 57.8±11.7 mm; p=0.016), higher Charlson Comorbidity Index (CCI) (32.3% versus 25.1% ≥6; p=0.034), and increased rates of rupture (8.2% versus 3.8%; p=0.047). Sarcopenic and nonsarcopenic patients had no difference in 30-day morbidity (8.5% versus 8.5%; p=0.991) or mortality (3.7% versus 0.9%; p=0.07). Univariate analysis demonstrated age, sarcopenia, myosteatosis, CCI, and BMI to be associated with long-term survival. There was no correlation between BMI and sarcopenia. Both sarcopenia and myosteatosis resulted in decreased one-, three-, and five-year survivals compared to their counterparts. On multivariate analysis sarcopenia is independently associated with survival, conferring a 1.6-fold increase in death (p=0.04). The combination of sarcopenia plus myosteatosis doubled the risk of death compared to sarcopenia alone. Conclusions This is the first study to demonstrate that over half of all patients undergoing AAA repair are sarcopenic, a condition associated with increased mortality. Sarcopenia with myosteatosis is associated with double the mortality of sarcopenia alone. CT scan, but not BMI, accurately identifies sarcopenia and myosteatosis. Defining the mechanisms through which sarcopenia contributes to late death after AAA repair is critical to developing novel interventions that may improve survival in this high risk population

    RPL24: a potential therapeutic target whose depletion or acetylation inhibits polysome assembly and cancer cell growth.

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    Partial loss of large ribosomal subunit protein 24 (RPL24) function is known to protect mice against Akt or Myc-driven cancers, in part via translational inhibition of a subset of cap(eIF4E)-dependently translated mRNAs. The role of RPL24 in human malignancies is unknown. By analyzing a public dataset of matched human breast cancers and normal mammary tissue, we found that breast cancers express significantly more RPL24 than matched normal breast samples. Depletion of RPL24 in breast cancer cells by \u3e70% reduced cell viability by 80% and decreased protein expression of the eIF4E-dependently translated proteins cyclin D1 (75%), survivin (46%) and NBS1 (30%) without altering GAPDH or beta-tubulin levels. RPL24 knockdown also reduced 80S subunit levels relative to 40S and 60S levels. These effects on expression of eIF4E-dependent proteins and ribosome assembly were mimicked by 2-24 h treatment with the pan-HDACi, trichostatin A (TSA), which induced acetylation of 15 different polysome-associated proteins including RPL24. Furthermore, HDAC6-selective inhibition or HDAC6 knockdown induced ribosomal protein acetylation. Via mass spectrometry, we found that 60S-associated, but not, polysome-associated, RPL24 undergoes HDACi-induced acetylation on K27. Thus, RPL24 K27 acetylation may play a role in ribosome assembly. These findings point toward a novel acetylation-dependent polysome assembly mechanism regulating tumorigenesis

    Mitochondrial calcium exchange links metabolism with the epigenome to control cellular differentiation.

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    Fibroblast to myofibroblast differentiation is crucial for the initial healing response but excessive myofibroblast activation leads to pathological fibrosis. Therefore, it is imperative to understand the mechanisms underlying myofibroblast formation. Here we report that mitochondrial calcium (mCa2+) signaling is a regulatory mechanism in myofibroblast differentiation and fibrosis. We demonstrate that fibrotic signaling alters gating of the mitochondrial calcium uniporter (mtCU) in a MICU1-dependent fashion to reduce mCa2+ uptake and induce coordinated changes in metabolism, i.e., increased glycolysis feeding anabolic pathways and glutaminolysis yielding increased α-ketoglutarate (αKG) bioavailability. mCa2+-dependent metabolic reprogramming leads to the activation of αKG-dependent histone demethylases, enhancing chromatin accessibility in loci specific to the myofibroblast gene program, resulting in differentiation. Our results uncover an important role for the mtCU beyond metabolic regulation and cell death and demonstrate that mCa2+ signaling regulates the epigenome to influence cellular differentiation

    Modeling the Probability of Overlap Between Marine Fish Distributions and Marine Renewable Energy Infrastructure Using Acoustic Telemetry Data

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    Understanding the spatiotemporal distributions of migratory marine species at marine renewable energy sites is a crucial step towards assessing the potential impacts of tidal stream turbines and related infrastructure upon these species. However, the dynamic marine conditions that make tidal channels attractive for marine renewable power development also make it difficult to identify and follow species of marine fishes with existing technologies such as hydroacoustics and optical cameras. Acoustic telemetry can resolve some of these problems. Acoustic tags provide unique individual ID codes at an ultrasonic frequency, which are then detected and recorded by acoustic receivers deployed in the area of interest. By matching detection locations of fish species with environmental conditions at proposed sites for tidal energy infrastructure, species distribution models can be developed to predict the probability of species occurrence at sites of current and planned tidal power development. This information can be used to develop statistically robust encounter rate models to aid in quantifying the risk of tidal power development to migratory fish species. We used this approach to develop a predictive model of striped bass (Morone saxatilis) distribution within Minas Passage in the upper Bay of Fundy, Nova Scotia. Model results suggested increased probability of striped bass presence in Minas Passage during late ebb tide conditions and at relatively high water temperatures. We demonstrate the potential utility of species distribution modeling of acoustic tag detections in predicting interactions with renewable energy infrastructure, and show the importance of physical oceanographic variables influencing species distributions in a highly dynamic marine environment
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