Wideband (15–260 kHz) acoustic volume backscattering spectra of Northern krill (Meganyctiphanes norvegica) and butterfish (Peprilus triacanthus)

This paper is not subject to U.S. copyright. The definitive version was published in ICES Journal of Marine Science 74 (2017): 2249–2261, doi:10.1093/icesjms/fsx050.Measurements of acoustic backscatter made over a wide frequency band have the potential for improved classification relative to traditional narrowband methods, by characterizing more fully the frequency response of scatterers. In January 2014, five wideband transceivers [Simrad EK80 Wideband Transceivers (WBTs)] and split-beam transducers with nominal centre frequencies of 18, 38, 70, 120, and 200 kHz were used to collect acoustic data spanning a nearly continuous 15–260 kHz bandwidth. The acoustic samples were from ca. 2 m below the surface to the seabed in an area along the US continental shelf break. Bottom trawls and zooplankton nets were also used to sample scatterers contributing to selected features of the acoustic backscatter. Measurements of frequency-dependent volume backscattering strength (i.e. volume backscattering spectra) from aggregations of euphausiids (mostly Northern krill, Meganyctiphanes norvegica) clearly resolved the transition from Rayleigh to geometric scattering, consistent with modelled backscatter from the type and length of animals sampled with bongo nets. Volume backscattering spectra from aggregations dominated by butterfish (Peprilus triacanthus) revealed a frequency response that was suggestive of superimposed scattering by soft tissue and bone. Backscatter predicted by Kirchhoff ray mode models of butterfish corresponded to trends in the measured spectra, supporting the assumption that acoustic scattering by butterfish is dominated by soft tissue and vertebrae.NOAA Advanced Sampling Technology Working Group (ASTWG) provided support for this project. GLL was partially supported by NOAA Cooperative Agreements NA09OAR4320129 and NA14OAR4320158 through the NOAA Fisheries Quantitative Ecology and Socioeconomics Training (QUEST) programme

Exploiting signal processing approaches for broadband echosounders

© International Council for the Exploration of the Sea, 2017. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in ICES Journal of Marine Science 74 (2017): 2262–2275, doi:10.1093/icesjms/fsx155.Broadband echosounders, which transmit frequency-modulated pulses, increase the spectral characterization of targets relative to narrowband echosounders, which typically transmit single-frequency pulses, and also increase the range resolution through broadband matched-filter signal processing approaches. However, the increased range resolution does not necessarily lead to improved detection and characterization of targets close to boundaries due to the presence of undesirable signal processing side lobes. The standard approach to mitigating the impact of processing side lobes is to transmit tapered signals, which has the consequence of also reducing spectral information. To address this, different broadband signal processing approaches are explored using data collected in a large tank with both a Kongsberg–Simrad EK80 scientific echosounder with a combination of single- and split-beam transducers with nominal centre frequencies of 18, 38, 70, 120, 200, and 333 kHz, and with a single-beam custom-built echosounder spanning the frequency band from 130 to 195 kHz. It is shown that improved detection and characterization of targets close to boundaries can be achieved by using modified replica signals in the matched filter processing. An additional benefit to using broadband echosounders involves exploiting the frequency dependence of the beam pattern to calibrate single-beam broadband echosounders using an off-axis calibration sphere.This research was supported by the NOAA Office of Science and Technology, Advanced Sampling Technology Working Group. G.L.L. was partially supported by NOAA Cooperative Agreements NA09OAR4320129 and NA14OAR4320158 through the NOAA Fisheries Quantitative Ecology and Socieconomics Training (QUEST) program. A.C.L. was partially supported through the Office of Naval Research Ocean Acoustics Program

The emergence of the nicotinamide riboside kinases in the regulation of NAD+ metabolism

The concept of replenishing or elevating NAD+availability to combat metabolic disease and ageing is an area of intense research. This has led to a need to define the endogenous regulatory pathways and mechanisms cells and tissues utilise to maximise NAD+availability such that strategies to intervene in the clinical setting are able to be fully realised. This review discusses the importance of different salvage pathways involved in metabolising the vitamin B3 class of NAD+precursor molecules, with a particular focus on the recently identified nicotinamide riboside kinase pathway at both a tissue-specific and systemic level.</jats:p

Lysine-specific demethylase 1 promotes brown adipose tissue thermogenesis via repressing glucocorticoid activation

Brown adipocytes display phenotypic plasticity, as they can switch between the active states of fatty acid oxidation and energy dissipation versus a more dormant state. Cold exposure or β-adrenergic stimulation favors the active thermogenic state, whereas sympathetic denervation or glucocorticoid administration promotes more lipid accumulation. Our understanding of the molecular mechanisms underlying these switches is incomplete. Here we found that LSD1 (lysine-specific demethylase 1), a histone demethylase, regulates brown adipocyte metabolism in two ways. On the one hand, LSD1 associates with PRDM16 to repress expression of white fat-selective genes. On the other hand, LSD1 represses HSD11B1 (hydroxysteroid 11-β-dehydrogenase isozyme 1), a key glucocorticoid-activating enzyme, independently from PRDM16. Adipose-specific ablation of LSD1 impaired mitochondrial fatty acid oxidation capacity of the brown adipose tissue, reduced whole-body energy expenditure, and increased fat deposition, which can be significantly alleviated by simultaneously deleting HSD11B1. These findings establish a novel regulatory pathway connecting histone modification and hormone activation with mitochondrial oxidative capacity and whole-body energy homeostasis

Determining dominant scatterers of sound in mixed zooplankton populations

Author Posting. © Acoustical Society of America, 2007. This article is posted here by permission of Acoustical Society of America for personal use, not for redistribution. The definitive version was published in Journal of the Acoustical Society of America 122 (2007): 3304-3326, doi:10.1121/1.2793613.High-frequency acoustic scattering techniques have been used to investigate dominant scatterers in mixed zooplankton populations. Volume backscattering was measured in the Gulf of Maine at 43, 120, 200, and 420 kHz. Zooplankton composition and size were determined using net and video sampling techniques, and water properties were determined using conductivity, temperature, and depth sensors. Dominant scatterers have been identified using recently developed scattering models for zooplankton and microstructure. Microstructure generally did not contribute to the scattering. At certain locations, gas-bearing zooplankton, that account for a small fraction of the total abundance and biomass, dominated the scattering at all frequencies. At these locations, acoustically inferred size agreed well with size determined from the net samples. Significant differences between the acoustic, net, and video estimates of abundance for these zooplankton are most likely due to limitations of the net and video techniques. No other type of biological scatterer ever dominated the scattering at all frequencies. Copepods, fluid-like zooplankton that account for most of the abundance and biomass, dominated at select locations only at the highest frequencies. At these locations, acoustically inferred abundance agreed well with net and video estimates. A general approach for the difficult problem of interpreting high-frequency acoustic scattering in mixed zooplankton populations is described.This research was supported in part by the U.S. GLOBEC program, NOAA (Grant nos. NA17RJ1223 and NA67RJ0148), the James S. Cole and Cecily C. Selby Endowed Funds, the Penzance Endowed Fund for Support of Assistant Scientists, and the Adams Chair at the Woods Hole Oceanographic Institution. A selected number of focused experiments were also funded by the ONR (Grant No. N00014-98-1-0362)

11 beta-hydroxysteroid dehydrogenase type 1 regulates glucocorticoid-induced insulin resistance in skeletal muscle

OBJECTIVE: Glucocorticoid excess is characterized by increased adiposity, skeletal myopathy, and insulin resistance, but the precise molecular mechanisms are unknown. Within skeletal muscle, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts cortisone (11-dehydrocorticosterone in rodents) to active cortisol (corticosterone in rodents). We aimed to determine the mechanisms underpinning glucocorticoid-induced insulin resistance in skeletal muscle and indentify how 11beta-HSD1 inhibitors improve insulin sensitivity. \ud RESEARCH DESIGN AND METHODS: Rodent and human cell cultures, whole-tissue explants, and animal models were used to determine the impact of glucocorticoids and selective 11beta-HSD1 inhibition upon insulin signaling and action. \ud RESULTS: Dexamethasone decreased insulin-stimulated glucose uptake, decreased IRS1 mRNA and protein expression, and increased inactivating pSer$^{307}$ insulin receptor substrate (IRS)-1. 11beta-HSD1 activity and expression were observed in human and rodent myotubes and muscle explants. Activity was predominantly oxo-reductase, generating active glucocorticoid. A1 (selective 11beta-HSD1 inhibitor) abolished enzyme activity and blocked the increase in pSer$^{307}$ IRS1 and reduction in total IRS1 protein after treatment with 11DHC but not corticosterone. In C57Bl6/J mice, the selective 11beta-HSD1 inhibitor, A2, decreased fasting blood glucose levels and improved insulin sensitivity. In KK mice treated with A2, skeletal muscle pSer$^{307}$ IRS1 decreased and pThr$^{308}$ Akt/PKB increased. In addition, A2 decreased both lipogenic and lipolytic gene expression.\ud CONCLUSIONS: Prereceptor facilitation of glucocorticoid action via 11beta-HSD1 increases pSer$^{307}$ IRS1 and may be crucial in mediating insulin resistance in skeletal muscle. Selective 11beta-HSD1 inhibition decreases pSer$^{307}$ IRS1, increases pThr$^{308}$ Akt/PKB, and decreases lipogenic and lipolytic gene expression that may represent an important mechanism underpinning their insulin-sensitizing action