Presynaptic facilitation at the crayfish neuromuscular junction: Role of calcium-activated potassium conductance

Membrane potential was recorded intracellularly near presynaptic terminals of the excitor axon of the crayfish opener neuromuscular junction (NMJ), while transmitter release was recorded postsynaptically. This study focused on the effects of a presynaptic calcium-activated potassium conductance, gK(Ca), on the transmitter release evoked by single and paired depolarizing current pulses. Blocking gK(Ca) by adding tetraethylammonium ion (TEA; 5-20 mM) to a solution containing tetrodotoxin and aminopyridines caused the relation between presynaptic potential and transmitter release to steepen and shift to less depolarized potentials. When two depolarizing current pulses were applied at 20-ms intervals with gK(Ca) not blocked, the presynaptic voltage change to the second (test) pulse was inversely related to the amplitude of the first (conditioning) pulse. This effect of the conditioning prepulse on the response to the test pulse was eliminated by 20 mM TEA and by solutions containing 0 mM Ca2+/1 mM EGTA, suggesting that the reduction in the amplitude of the test pulse was due to activation of gK(Ca) by calcium remaining from the conditioning pulse. In the absence of TEA, facilitation of transmitter release evoked by a test pulse increased as the conditioning pulse grew from -40 to -20 mV, but then decreased with further increase in the conditioning depolarization. A similar nonmonotonic relationship between facilitation and the amplitude of the conditioning depolarization was reported in previous studies using extracellular recording, and interpreted as supporting an additional voltagedependent step in the activation of transmitter release. We suggest that this result was due instead to activation of a gK(Ca) by the conditioning depolarization, since facilitation of transmitter release increased monotonically with the amplitude of the conditioning depolarization, and the early time course of the decay of facilitation was prolonged when gK(Ca) was blocked. The different time courses for decay of the presynaptic potential (20 ms) and facilitation (> 50 ms) suggest either that residual free calcium does not account for facilitation at the crayfish NMJ or that the transmitter release mechanism has a markedly higher affinity or stoichiometry for internal free calcium than does g K(Ca). Finally, our data suggest that the calcium channels responsible for transmitter release at the crayfish NMJ are not of the L, N, or T type.This work was partially supported by NIAAA grant AA0776 to G. D. Bittner.Neuroscienc

Lifting of Ir{100} reconstruction by CO adsorption: An ab initio study

The adsorption of CO on unreconstructed and reconstructed Ir{100} has been studied, using a combination of density functional theory and thermodynamics, to determine the relative stability of the two phases as a function of CO coverage, temperature and pressure. We obtain good agreement with experimentaldata. At zero temperature, the (1X5) reconstruction becomes less stable than the unreconstructed (1X1) surface when the CO coverage exceeds a critical value of 0.09 ML. The interaction between CO molecules is found to be repulsive on the reconstructed surface, but attractive on the unreconstructed, explaining the experimental observation of high CO coverage on growing (1X1) islands. At all temperatures and pressures, we find only two possible stable states: 0.05 ML CO c(2X2) overlayer on the (1X1) substrate, and the clean (1$\times$5) reconstructed surface.Comment: 31 page

Genomics-Integrated Breeding for Carotenoids and Folates in Staple Cereal Grains to Reduce Malnutrition

Globally, two billion people suffer from micronutrient deficiencies. Cereal grains provide more than 50% of the daily requirement of calories in human diets, but they often fail to provide adequate essential minerals and vitamins. Cereal crop production in developing countries achieved remarkable yield gains through the efforts of the Green Revolution (117% in rice, 30% in wheat, 530% in maize, and 188% in pearl millet). However, modern varieties are often deficient in essential micronutrients compared to traditional varieties and land races. Breeding for nutritional quality in staple cereals is a challenging task; however, biofortification initiatives combined with genomic tools increase the feasibility. Current biofortification breeding activities include improving rice (for zinc), wheat (for zinc), maize (for provitamin A), and pearl millet (for iron and zinc). Biofortification is a sustainable approach to enrich staple cereals with provitamin A, carotenoids, and folates. Significant genetic variation has been found for provitamin A (96–850 mg and 12–1780 mg in 100 g in wheat and maize, respectively), carotenoids (558–6730 mg in maize), and folates in rice (11–51 mg) and wheat (32.3–89.1 mg) in 100 g. This indicates the prospects for biofortification breeding. Several QTLs associated with carotenoids and folates have been identified in major cereals, and the most promising of these are presented here. Breeding for essential nutrition should be a core objective of next-generation crop breeding. This review synthesizes the available literature on folates, provitamin A, and carotenoids in rice, wheat, maize, and pearl millet, including genetic variation, trait discovery, QTL identification, gene introgressions, and the strategy of genomics-assisted biofortification for these traits. Recent evidence shows that genomics-assisted breeding for grain nutrition in rice, wheat, maize, and pearl millet crops have good potential to aid in the alleviation of micronutrient malnutrition in many developing countries

Primary stroke prevention worldwide : translating evidence into action

Funding Information: The stroke services survey reported in this publication was partly supported by World Stroke Organization and Auckland University of Technology. VLF was partly supported by the grants received from the Health Research Council of New Zealand. MOO was supported by the US National Institutes of Health (SIREN U54 HG007479) under the H3Africa initiative and SIBS Genomics (R01NS107900, R01NS107900-02S1, R01NS115944-01, 3U24HG009780-03S5, and 1R01NS114045-01), Sub-Saharan Africa Conference on Stroke Conference (1R13NS115395-01A1), and Training Africans to Lead and Execute Neurological Trials & Studies (D43TW012030). AGT was supported by the Australian National Health and Medical Research Council. SLG was supported by a National Heart Foundation of Australia Future Leader Fellowship and an Australian National Health and Medical Research Council synergy grant. We thank Anita Arsovska (University Clinic of Neurology, Skopje, North Macedonia), Manoj Bohara (HAMS Hospital, Kathmandu, Nepal), Denis ?erimagi? (Poliklinika Glavi?, Dubrovnik, Croatia), Manuel Correia (Hospital de Santo Ant?nio, Porto, Portugal), Daissy Liliana Mora Cuervo (Hospital Moinhos de Vento, Porto Alegre, Brazil), Anna Cz?onkowska (Institute of Psychiatry and Neurology, Warsaw, Poland), Gloria Ekeng (Stroke Care International, Dartford, UK), Jo?o Sargento-Freitas (Centro Hospitalar e Universit?rio de Coimbra, Coimbra, Portugal), Yuriy Flomin (MC Universal Clinic Oberig, Kyiv, Ukraine), Mehari Gebreyohanns (UT Southwestern Medical Centre, Dallas, TX, USA), Ivete Pillo Gon?alves (Hospital S?o Jos? do Avai, Itaperuna, Brazil), Claiborne Johnston (Dell Medical School, University of Texas, Austin, TX, USA), Kristaps Jurj?ns (P Stradins Clinical University Hospital, Riga, Latvia), Rizwan Kalani (University of Washington, Seattle, WA, USA), Grzegorz Kozera (Medical University of Gda?sk, Gda?sk, Poland), Kursad Kutluk (Dokuz Eylul University, ?zmir, Turkey), Branko Malojcic (University Hospital Centre Zagreb, Zagreb, Croatia), Micha? Maluchnik (Ministry of Health, Warsaw, Poland), Evija Migl?ne (P Stradins Clinical University Hospital, Riga, Latvia), Cassandra Ocampo (University of Botswana, Princess Marina Hospital, Botswana), Louise Shaw (Royal United Hospitals Bath NHS Foundation Trust, Bath, UK), Lekhjung Thapa (Upendra Devkota Memorial-National Institute of Neurological and Allied Sciences, Kathmandu, Nepal), Bogdan Wojtyniak (National Institute of Public Health, Warsaw, Poland), Jie Yang (First Affiliated Hospital of Chengdu Medical College, Chengdu, China), and Tomasz Zdrojewski (Medical University of Gda?sk, Gda?sk, Poland) for their comments on early draft of the manuscript. The views expressed in this article are solely the responsibility of the authors and they do not necessarily reflect the views, decisions, or policies of the institution with which they are affiliated. We thank WSO for funding. The funder had no role in the design, data collection, analysis and interpretation of the study results, writing of the report, or the decision to submit the study results for publication. Funding Information: The stroke services survey reported in this publication was partly supported by World Stroke Organization and Auckland University of Technology. VLF was partly supported by the grants received from the Health Research Council of New Zealand. MOO was supported by the US National Institutes of Health (SIREN U54 HG007479) under the H3Africa initiative and SIBS Genomics (R01NS107900, R01NS107900-02S1, R01NS115944-01, 3U24HG009780-03S5, and 1R01NS114045-01), Sub-Saharan Africa Conference on Stroke Conference (1R13NS115395-01A1), and Training Africans to Lead and Execute Neurological Trials & Studies (D43TW012030). AGT was supported by the Australian National Health and Medical Research Council. SLG was supported by a National Heart Foundation of Australia Future Leader Fellowship and an Australian National Health and Medical Research Council synergy grant. We thank Anita Arsovska (University Clinic of Neurology, Skopje, North Macedonia), Manoj Bohara (HAMS Hospital, Kathmandu, Nepal), Denis Čerimagić (Poliklinika Glavić, Dubrovnik, Croatia), Manuel Correia (Hospital de Santo António, Porto, Portugal), Daissy Liliana Mora Cuervo (Hospital Moinhos de Vento, Porto Alegre, Brazil), Anna Członkowska (Institute of Psychiatry and Neurology, Warsaw, Poland), Gloria Ekeng (Stroke Care International, Dartford, UK), João Sargento-Freitas (Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal), Yuriy Flomin (MC Universal Clinic Oberig, Kyiv, Ukraine), Mehari Gebreyohanns (UT Southwestern Medical Centre, Dallas, TX, USA), Ivete Pillo Gonçalves (Hospital São José do Avai, Itaperuna, Brazil), Claiborne Johnston (Dell Medical School, University of Texas, Austin, TX, USA), Kristaps Jurjāns (P Stradins Clinical University Hospital, Riga, Latvia), Rizwan Kalani (University of Washington, Seattle, WA, USA), Grzegorz Kozera (Medical University of Gdańsk, Gdańsk, Poland), Kursad Kutluk (Dokuz Eylul University, İzmir, Turkey), Branko Malojcic (University Hospital Centre Zagreb, Zagreb, Croatia), Michał Maluchnik (Ministry of Health, Warsaw, Poland), Evija Miglāne (P Stradins Clinical University Hospital, Riga, Latvia), Cassandra Ocampo (University of Botswana, Princess Marina Hospital, Botswana), Louise Shaw (Royal United Hospitals Bath NHS Foundation Trust, Bath, UK), Lekhjung Thapa (Upendra Devkota Memorial-National Institute of Neurological and Allied Sciences, Kathmandu, Nepal), Bogdan Wojtyniak (National Institute of Public Health, Warsaw, Poland), Jie Yang (First Affiliated Hospital of Chengdu Medical College, Chengdu, China), and Tomasz Zdrojewski (Medical University of Gdańsk, Gdańsk, Poland) for their comments on early draft of the manuscript. The views expressed in this article are solely the responsibility of the authors and they do not necessarily reflect the views, decisions, or policies of the institution with which they are affiliated. We thank WSO for funding. The funder had no role in the design, data collection, analysis and interpretation of the study results, writing of the report, or the decision to submit the study results for publication. Funding Information: VLF declares that the PreventS web app and Stroke Riskometer app are owned and copyrighted by Auckland University of Technology; has received grants from the Brain Research New Zealand Centre of Research Excellence (16/STH/36), Australian National Health and Medical Research Council (NHMRC; APP1182071), and World Stroke Organization (WSO); is an executive committee member of WSO, honorary medical director of Stroke Central New Zealand, and CEO of New Zealand Stroke Education charitable Trust. AGT declares funding from NHMRC (GNT1042600, GNT1122455, GNT1171966, GNT1143155, and GNT1182017), Stroke Foundation Australia (SG1807), and Heart Foundation Australia (VG102282); and board membership of the Stroke Foundation (Australia). SLG is funded by the National Health Foundation of Australia (Future Leader Fellowship 102061) and NHMRC (GNT1182071, GNT1143155, and GNT1128373). RM is supported by the Implementation Research Network in Stroke Care Quality of the European Cooperation in Science and Technology (project CA18118) and by the IRIS-TEPUS project from the inter-excellence inter-cost programme of the Ministry of Education, Youth and Sports of the Czech Republic (project LTC20051). BN declares receiving fees for data management committee work for SOCRATES and THALES trials for AstraZeneca and fees for data management committee work for NAVIGATE-ESUS trial from Bayer. All other authors declare no competing interests. Publisher Copyright: © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseStroke is the second leading cause of death and the third leading cause of disability worldwide and its burden is increasing rapidly in low-income and middle-income countries, many of which are unable to face the challenges it imposes. In this Health Policy paper on primary stroke prevention, we provide an overview of the current situation regarding primary prevention services, estimate the cost of stroke and stroke prevention, and identify deficiencies in existing guidelines and gaps in primary prevention. We also offer a set of pragmatic solutions for implementation of primary stroke prevention, with an emphasis on the role of governments and population-wide strategies, including task-shifting and sharing and health system re-engineering. Implementation of primary stroke prevention involves patients, health professionals, funders, policy makers, implementation partners, and the entire population along the life course.publishersversionPeer reviewe

Unexpected circular radio objects at high Galactic latitude

Large scale structure and cosmolog

Radio continuum sources behind the Large Magellanic Cloud

We present a comprehensive multifrequency catalogue of radio sources behind the Large Magellanic Cloud (LMC) between 0.2 and 20 GHz, gathered from a combination of new and legacy radio continuum surveys. This catalogue covers an area of ∼144 deg2 at angular resolutions from 45 arcsec to ∼3 arcmin. We find 6434 discrete radio sources in total, of which 3789 are detected at two or more radio frequencies. We estimate the median spectral index (α; where Sv ∼ να) of α = −0.89 and mean of −0.88 ± 0.48 for 3636 sources detected exclusively at two frequencies (0.843 and 1.384 GHz) with similar resolution [full width at half-maximum (FWHM) ∼40–45 arcsec]. The large frequency range of the surveys makes it an effective tool to investigate Gigahertz Peak Spectrum (GPS), Compact Steep Spectrum (CSS), and Infrared Faint Radio Source (IFRS) populations within our sample. We find 10 GPS candidates with peak frequencies near 5 GHz, from which we estimate their linear size. 1866 sources from our catalogue are CSS candidates with α  < −0.8. We found six candidates for High Frequency Peaker (HFP) sources, whose radio fluxes peak above 5 GHz and no sources with unconstrained peaks and α  > 0.5. We found optical counterparts for 343 of the radio continuum sources, of which 128 have a redshift measurement. Finally, we investigate the population of 123 IFRSs found in this study

Isolation and Characterization of Dually Reactive Strains of Group A Rotavirus from Hospitalized Children

Seven rotavirus strains dually reactive to serotype G1- and G2-specific monoclonal antibodies (MAbs) from hospitalized children with rotavirus diarrhea were culture adapted. Six strains were neutralized with G1 antiserum to a higher titer than that of G2, and one was neutralized with G1 and G2 antisera to equal titers. Of these, four strains were also neutralized with G6 antiserum. Five strains with short RNA pattern could not be serotyped, and the remaining two strains with long RNA pattern were serotyped as G1 strains. In addition, two strains showing dual reactivity to G2 and G4 MAbs and one G2-like strain from a nontypeable specimen were isolated. The dual reactivity of the isolates could not be attributed to mixed infections