Effect of different degraded protein balances (OEB) on the performance of beef bulls and on digestibility and rumen fermentation in sheep

A total of 125 non-double-muscled Belgian Blue finishing bulls (liveweight range 375-620 kg) were used to investigate the effect of different levels of degraded protein balance in the rumen (OEB) -2, -7, -16 and -22 g/kg DM on animal performance, with the dietary content of true protein digested in the small intestine (DVE) fixed at 80 g/kg. Lower OEB levels significantly reduced daily liveweight gain from 1.57 to 1.39 kg during the first 84 days of the experiment, but not during the subsequent part. For the whole experiment, daily liveweight gain decreased from 1.40 to 1.32 kg but the difference was not significant. Intake of DM, DVE and NE for finishing was not modified by OEB level, while CP intake was reduced and OEB deficit was increased. An OEB level of -22 g/kg DM resulted in a significantly unfavourable conversion of DM and NE during the initial months (11.3 and 11.5% compared with OEB = -2 g/kg DM, respectively). For the total period the conversion of DM and NE was still less favourable, but the differences were not significant. There was a nominal decrease in cold carcass weight and dressing percentage when OEB level decreased, but the effect was not significant. The effect of different OEB levels on digestibility and rumen fermentation was investigated in a separate experiment with wethers. Apparent protein digestibility was reduced from 74.2 to 68.9% when OEB level decreased. Rumen pH and concentrations and molar percentages of volatile fatty acids were not altered by OEB level. Ammonia concentration was only reduced by a lower OEB level at 7 h after feeding. Because of a nominal reduction in daily liveweight gain, feed efficiency, carcass weight, dressing percentage and carcass conformation with decreasing OEB level, it is advisable not to feed less than -16 g OEB/kg DM in diets with 80 g DVE/kg DM to Belgian Blue non-double-muscled finishing bulls from 375 kg onwards. This tolerable OEB deficit is larger than proposed to avoid protein overfeeding

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

Checking the cycle by ERRβ splice variants

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Evaluation of the nutritive value of maize silages using a gas production technique

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Protein evaluation of cattle compound feeds: comparison of in sacco measurements and tabular values

The supply of true protein to the small intestine (DVE) and the degraded protein balance (OEB) of 29 experimental compound feeds were estimated in the rumen and intestine of dairy cows (reference), using the nylon bag technique. DVE and OEB were also calculated from tabulated values of the ingredients, taken from the Dutch CVB-tables, assuming additive effects. Reference DVE was on average 11 g/kg DM lower and OEB 6 g/kg DM higher than tabulated values, resulting from a higher rumen degradability of protein (-5.5 percentage units) and lower intestinal digestibility of rumen undegradable protein (-2.0 percentage units) and a lower rumen degradability of starch (+5.8% units) and DOM-content (+27 g/kg DM). The possible causes of these differences are discussed. After elimination of systemic differences, residual errors between reference and tabular values amounted to 5.9 and 14.9% for DVE and OEB, respectively. It is concluded that a reasonable relation exists between DVE- and OEB-content of compound feeds based on tabular values for the ingredients and those calculated from in sacco measurements

Potential of solubility, enzymatic methods and NIRS to predict in situ rumen escape protein

The percentage of feed protein escaping rumen degradation was measured by the in situ method (%EPsitu) for 29 compound feeds, untreated and formaldehyde-treated soyabean meal and 12 forages: 3 grass silages, 2 maize silages, fresh grass, grass hay, fodder beets, fresh potatoes, ensiled beet pulp, chopped ear-maize silage and brewers' grains. Loss of particles through bag pores was determined by the difference between the washable fraction (W) and the fraction soluble in borate-phosphate buffer at pH 6.7 (S). W - S was most pronounced for compound feeds (on average 14.4 percentage units), for brewers' grains and maize silages. A correction of %EPsitu, assuming that W - S degrades like the potentially degradable fraction, was not appropriate. Solubility in borate-phosphate buffer after 1 h, enzymic degradability by protease from Streptomyces griseus or ficin after 1, 6 and 24 h and near infrared reflectance spectroscopy (NIRS) (for compound feeds alone) were examined as a routine method to predict %EPsitu. With the buffer and S. griseus the effect of pH (6.7 vs. 8.0) and at pH 8.0 the effect of amount of substrate (500-mg sample vs. 20 mg N) were tested. With ficin, 500-mg samples were incubated at pH 6.7. Predictions were better when compound feeds and forages were considered separately. However, the best in vitro method was different for the 2 feed categories, being solubility in buffer for the compound feeds and enzymic degradation of a constant amount of protein with S. griseus at pH 8.0 for forages. NIRS showed potential to predict %EPsitu of compound feeds, but needs more reference samples. The Dutch feed tables appeared more accurate than the best in vitro method for compound feeds, but was too inaccurate for some forages like fodder beets, maize silage and ear-maize silage

Expression of the orphan nuclear receptor ERRalpha is under circadian regulation in estrogen-responsive tissues

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Dimerization is required for transactivation by estrogen-related (ERR) orphan receptors: evidence from amphioxus ERR

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Cloning and developmental expression of five estrogen-receptor related genes in the zebrafish

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Amphi-COUP-TF, a nuclear orphan receptor of the lancelet Branchiostoma floridae, is implicated in retinoic acid signaling pathways.

International audienceIn vertebrates, the orphan nuclear receptors of the COUP-TF group function as negative transcriptionalregulators that inhibit the hormonal induction of targetgenes mediated by classical members of the nuclear hor-mone superfamily, such as the retinoic acid receptors(RARs) or the thyroid hormone receptors (TRs). To in-vestigate the evolutionary conservation of the roles of COUP-TF receptors as negative regulators in the retinoidand thyroid hormone pathways, we have characterizedAmphiCOUP-TF, the homologue of COUP-TFI andCOUP-TFII, in the chordate amphioxus ( Branchiostoma floridae ), the closest living invertebrate relative of thevertebrates. Electrophoretic mobility shift assays(EMSA) showed that AmphiCOUP-TF binds to a widevariety of response elements, as do its vertebrate homo-logues. Furthermore, AmphiCOUP-TF is a transcription-al repressor that strongly inhibits retinoic acid-mediatedtransactivation. In situ hybridizations revealed expres-sion of AmphiCOUP-TF in the nerve cord of late larvae,in a region corresponding to hindbrain and probably an-terior spinal cord. Although the amphioxus nerve cordappears unsegmented at the gross anatomical level, thispattern reflects segmentation at the cellular level withstripes of expressing cells occurring adjacent to the endsand the centers of each myotomal segment, which mayinclude visceral motor neurons and somatic motor neu-rons respectively, among other cells. A comparison of the expression pattern of AmphiCOUP-TF with those of its vertebrate homologues, suggests that the roles of COUP-TF in patterning of the nerve cord evolved priorto the split between the amphioxus and vertebrate lineag-es. Furthermore, in vitro data also suggest that Amphi-COUP-TF acts as a negative regulator of signalling byother nuclear receptors such as RAR, TR or ER