1,725,287 research outputs found

    UMNH:Mamm:4497

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    UMNH:Mamm:4497 Voucher specimen study ski

    FG-4497: a new target for acute respiratory distress syndrome?

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    The morbidity and mortality rates associated with acute respiratory distress syndrome (ARDS) remain high and the development of new therapeutic strategies is urgently required. Some pharmacological treatments, proposed or under evaluation for ARDS, seek to protect the endothelium and consequently mitigate fluid extravasation into the alveolar space. FG-4497 is a new compound which acts as a prolyl hydroxylase domain 2 inhibitor and mimics hypoxia in the activation of hypoxia-inducible factor-2α signaling, decreasing VE-cadherin phosphorylation and thus promoting integrity of adherens junctions. In this special report, we discuss the pharmacological characteristics of FG-4497, its effect on lung parenchyma and other organs and future perspectives in ARDS. In short, FG-4497 may be considered a novel pharmacological option targeting endothelial cell repair in lung diseases such as ARDS. Further experimental and clinical studies are warranted to better understand the mechanisms of action of FG-4497 in different types of lung injury

    Linked collectors and determiners for: Colección Hidrobiológica del Chocó.

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    Natural history specimen data linked to collectors and determiners held within, "Colección Hidrobiológica del Chocó". Claims or attributions were made on Bionomia by volunteer Scribes, <a href="http://bionomia.net/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd">https://bionomia.net/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd</a> using specimen data from the dataset aggregated by the Global Biodiversity Information Facility, <a href="https://gbif.org/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd">https://gbif.org/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd</a>. Formatted as a Frictionless Data package

    Linked collectors and determiners for: Colección Hidrobiológica del Chocó.

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    Natural history specimen data linked to collectors and determiners held within, "Colección Hidrobiológica del Chocó". Claims or attributions were made on Bionomia by volunteer Scribes, <a href="http://bionomia.net/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd">https://bionomia.net/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd</a> using specimen data from the dataset aggregated by the Global Biodiversity Information Facility, <a href="https://gbif.org/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd">https://gbif.org/dataset/13b4fdb0-92a0-4497-bc0a-16d2fdf806fd</a>. Formatted as a Frictionless Data package

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Linked collectors and determiners for: PaDIL.

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    Natural history specimen data linked to collectors and determiners held within, "PaDIL". Claims or attributions were made on Bionomia by volunteer Scribes, <a href="http://bionomia.net/dataset/e731a329-1fe3-4497-9e3c-24cb9235b5a1">https://bionomia.net/dataset/e731a329-1fe3-4497-9e3c-24cb9235b5a1</a> using specimen data from the dataset aggregated by the Global Biodiversity Information Facility, <a href="https://gbif.org/dataset/e731a329-1fe3-4497-9e3c-24cb9235b5a1">https://gbif.org/dataset/e731a329-1fe3-4497-9e3c-24cb9235b5a1</a>. Formatted as a Frictionless Data package

    Study of scale inhibitor SI-4497 effect on calcareous deposit

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    Calcareous deposits in water desalination generate serious problems and lead to considerable economic losses. The aim of this study is to investigate the inhibition of calcareous deposits using polyphosphonate (scale inhibitor SI-4497), which is an ideal additive for desalination operations. We studied the recovery rate of titanium electrode, in the presence and absence of this inhibitor, using chronoamperometry. A cathodic potential of –1.3 V/SCE (SCE – saturated calomel electrode) is used at 1,000 rpm and at 20°C, 40°C, 60°C, 80°C. Levich’s law is verified before and after 1 h of electrodeposition in presence of an inhibitor. It was found that electrode recovery decreases with the addition of 3.5 ppm polyphosphonate (scale inhibitor SI-4497), resulting in an efficiency of 63.65

    HIF-1α-stabilizing agent FG-4497 rescues human CD34+ cell mobilization in response to G-CSF in immunodeficient mice

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    Granulocyte colony-stimulating factor (G-CSF) is used routinely in the clinical setting to mobilize hematopoietic stem progenitor cells (HSPCs) into the patient's blood for collection and subsequent transplantation. However, a significant proportion of patients who have previously received chemotherapy or radiotherapy and require autologous HSPC transplantation cannot mobilize the minimal threshold of mobilized HSPCs to achieve rapid and successful hematopoietic reconstitution. Although several alternatives to the G-CSF regime have been tested, few are used in the clinical setting. We have shown previously in mice that administration of prolyl 4-hydroxylase domain enzyme (PHD) inhibitors, which stabilize hypoxiainducible factor (111F)-1 alpha, synergize with G-CSF in vivo to enhance mouse HSPC mobilization into blood, leading to enhanced engraftment via an HSPC-intrinsic mechanism. To evaluate whether PHD inhibitors could be used to enhance mobilization of human HSPCs, we humanized nonobese, diabetic severe combined immune-deficient Il2rg(-/-) mice by transplanting them with human umbilical cord blood CD34(+) HSPCs and then treating them with G-CSF with and without co-administration of the PHD inhibitor FG-4497. We observed that combination treatment with G-CSF and FG-4497 resulted in significant mobilization of human lineage-negative (Lin(-)) CD34(+) HSPCs and more primitive human Lin(-) CD34(+)CD38(-) HSPCs into blood and spleen, whereas mice treated with G-CSF alone did not mobilize human HSPCs significantly. These results suggest that the PHD inhibitor FG-4497 also increases human HSPC mobilization in a xenograft mouse model, suggesting the possibility of testing PHD inhibitors to boost HSPC mobilization in response to G-CSF in humans. Copyright (C) 2017 ISEH - International Society for Experimental Hematology. Published by Elsevier Inc
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