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  • 1
    Online Resource
    Online Resource
    Quality Assessment of Established and Emerging Blood Components for Transfusion
    Hindawi Limited ; 2016
    In:  Journal of Blood Transfusion Vol. 2016 ( 2016-12-14), p. 1-28
    Details
    In: Journal of Blood Transfusion, Hindawi Limited, Vol. 2016 ( 2016-12-14), p. 1-28
    Abstract: Blood is donated either as whole blood, with subsequent component processing, or through the use of apheresis devices that extract one or more components and return the rest of the donation to the donor. Blood component therapy supplanted whole blood transfusion in industrialized countries in the middle of the twentieth century and remains the standard of care for the majority of patients receiving a transfusion. Traditionally, blood has been processed into three main blood products: red blood cell concentrates; platelet concentrates; and transfusable plasma. Ensuring that these products are of high quality and that they deliver their intended benefits to patients throughout their shelf-life is a complex task. Further complexity has been added with the development of products stored under nonstandard conditions or subjected to additional manufacturing steps (e.g., cryopreserved platelets, irradiated red cells, and lyophilized plasma). Here we review established and emerging methodologies for assessing blood product quality and address controversies and uncertainties in this thriving and active field of investigation.
    Type of Medium: Online Resource
    ISSN: 2090-9187 , 2090-9195
    URL: Article
    DOI: 10.1155/2016/4860284
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2016
    detail.hit.zdb_id: 2658685-X
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  • 2
    Online Resource
    Online Resource
    Plasma and Plasma Protein Product Transfusion: A Canadian Blood Services Centre for Innovation Symposium
    Elsevier BV ; 2015
    In:  Transfusion Medicine Reviews Vol. 29, No. 3 ( 2015-07), p. 181-194
    Details
    In: Transfusion Medicine Reviews, Elsevier BV, Vol. 29, No. 3 ( 2015-07), p. 181-194
    Type of Medium: Online Resource
    ISSN: 0887-7963
    URL: Article
    DOI: 10.1016/j.tmrv.2015.03.003
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 2121215-6
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  • 3
    Online Resource
    Online Resource
    Whole blood treated with riboflavin and ultraviolet light: quality assessment of all blood components produced by the buffy coat method
    Wiley ; 2015
    In:  Transfusion Vol. 55, No. 4 ( 2015-04), p. 815-823
    Details
    In: Transfusion, Wiley, Vol. 55, No. 4 ( 2015-04), p. 815-823
    Abstract: Pathogen inactivation ( PI ) technologies are currently licensed for use with platelet ( PLT ) and plasma components. Treatment of whole blood ( WB ) would be of benefit to the blood banking community by saving time and costs compared to individual component treatment. However, no paired, pool‐and‐split study directly assessing the impact of WB PI on the subsequently produced components has yet been reported. Study Design and Methods In a “pool‐and‐split” study, WB either was treated with riboflavin and ultraviolet ( UV ) light or was kept untreated as control. The buffy coat ( BC ) method produced plasma, PLT , and red blood cell ( RBC ) components. PLT units arising from the untreated WB study arm were treated with riboflavin and UV light on day of production and compared to PLT concentrates ( PCs ) produced from the treated WB units. A panel of common in vitro variables for the three types of components was used to monitor quality throughout their respective storage periods. Results PCs derived from the WB PI treatment were of significantly better quality than treated PLT components for most variables. RBCs produced from the WB treatment deteriorated earlier during storage than untreated units. Plasma components showed a 3% to 44% loss in activity for several clotting factors. Conclusion Treatment of WB with riboflavin and UV before production of components by the BC method shows a negative impact on all three blood components. PLT units produced from PI ‐treated WB exhibited less damage compared to PLT component treatment.
    Type of Medium: Online Resource
    ISSN: 0041-1132 , 1537-2995
    URL: Issue
    URL: Article
    DOI: 10.1111/trf.v55.4
    DOI: 10.1111/trf.12895
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2018415-3
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  • 4
    Online Resource
    Online Resource
    Fluorous Analogue of Chloramine-T: Preparation, X-ray Structure Determination, and Use as an Oxidant for Radioiodination and s-Tetrazine Synthesis
    American Chemical Society (ACS) ; 2015
    In:  The Journal of Organic Chemistry Vol. 80, No. 14 ( 2015-07-17), p. 7117-7125
    Details
    In: The Journal of Organic Chemistry, American Chemical Society (ACS), Vol. 80, No. 14 ( 2015-07-17), p. 7117-7125
    Type of Medium: Online Resource
    ISSN: 0022-3263 , 1520-6904
    URL: Article
    DOI: 10.1021/acs.joc.5b00988
    RVK:
    VA 5350
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 2015
    detail.hit.zdb_id: 1472273-2
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  • 5
    Online Resource
    Online Resource
    Quality and Safety of Blood Products
    Hindawi Limited ; 2016
    In:  Journal of Blood Transfusion Vol. 2016 ( 2016-12-29), p. 1-2
    Details
    In: Journal of Blood Transfusion, Hindawi Limited, Vol. 2016 ( 2016-12-29), p. 1-2
    Type of Medium: Online Resource
    ISSN: 2090-9187 , 2090-9195
    URL: Article
    DOI: 10.1155/2016/2482157
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2016
    detail.hit.zdb_id: 2658685-X
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  • 6
    Online Resource
    Online Resource
    Deadly calcium influx could be one way TSP-1 kills red blood cells and promotes disease
    Springer Science and Business Media LLC ; 2020
    In:  Cell Communication and Signaling Vol. 18, No. 1 ( 2020-12)
    Details
    In: Cell Communication and Signaling, Springer Science and Business Media LLC, Vol. 18, No. 1 ( 2020-12)
    Abstract: Thrombospondin-1 (TSP-1), a Ca 2+ -binding trimeric glycoprotein secreted by multiple cell types, has been implicated in the pathophysiology of several clinical conditions. Signaling involving TSP-1, through its cognate receptor CD47, orchestrates a wide array of cellular functions including cytoskeletal organization, migration, cell-cell interaction, cell proliferation, autophagy, and apoptosis. In the present study, we investigated the impact of TSP-1/CD47 signaling on Ca 2+ dynamics, survival, and deformability of human red blood cells (RBCs). Methods Whole-cell patch-clamp was employed to examine transmembrane cation conductance. RBC intracellular Ca 2+ levels and multiple indices of RBC cell death were determined using cytofluorometry analysis. RBC morphology and microvesiculation were examined using imaging flow cytometry. RBC deformability was measured using laser-assisted optical rotational cell analyzer. Results Exposure of RBCs to recombinant human TSP-1 significantly increased RBC intracellular Ca 2+ levels. As judged by electrophysiology experiments, TSP-1 treatment elicited an amiloride-sensitive inward current alluding to a possible Ca 2+ influx via non-selective cation channels. Exogenous TSP-1 promoted microparticle shedding as well as enhancing Ca 2+ - and nitric oxide-mediated RBC cell death. Monoclonal (mouse IgG1) antibody-mediated CD47 ligation using 1F7 recapitulated the cell death-inducing effects of TSP-1. Furthermore, TSP-1 treatment altered RBC cell shape and stiffness (maximum elongation index). Conclusions Taken together, our data unravel a new role for TSP-1/CD47 signaling in mediating Ca 2+ influx into RBCs, a mechanism potentially contributing to their dysfunction in a variety of systemic diseases.
    Type of Medium: Online Resource
    ISSN: 1478-811X
    URL: Article
    URL: Article
    DOI: 10.1186/s12964-020-00651-5
    DOI: 10.21203/rs.3.rs-106694/v1
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2126315-2
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    The complete N-terminal extension of heparin cofactor II is required for maximal effectiveness as a thrombin exosite 1 ligand
    Springer Science and Business Media LLC ; 2013
    In:  BMC Biochemistry Vol. 14, No. 1 ( 2013-12)
    Details
    In: BMC Biochemistry, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2013-12)
    Abstract: Heparin cofactor II (HCII) is a circulating protease inhibitor, one which contains an N-terminal acidic extension (HCII 1-75) unique within the serpin superfamily. Deletion of HCII 1-75 greatly reduces the ability of glycosaminoglycans (GAGs) to accelerate the inhibition of thrombin, and abrogates HCII binding to thrombin exosite 1. While a minor portion of HCII 1-75 can be visualized in a crystallized HCII-thrombin S195A complex, the role of the rest of the extension is not well understood and the affinity of the HCII 1-75 interaction has not been quantitatively characterized. To address these issues, we expressed HCII 1-75 as a small, N-terminally hexahistidine-tagged polypeptide in E. coli. Results Immobilized purified HCII 1-75 bound active α-thrombin and active-site inhibited FPR-ck- or S195A-thrombin, but not exosite-1-disrupted γ T -thrombin, in microtiter plate assays. Biotinylated HCII 1-75 immobilized on streptavidin chips bound α-thrombin and FPR-ck-thrombin with similar K D values of 330-340 nM. HCII 1-75 competed thrombin binding to chip-immobilized HCII 1-75 more effectively than HCII 54-75 but less effectively than the C-terminal dodecapeptide of hirudin (mean K i values of 2.6, 8.5, and 0.29 μM, respectively). This superiority over HCII 54-75 was also demonstrated in plasma clotting assays and in competing the heparin-catalysed inhibition of thrombin by plasma-derived HCII; HCII 1-53 had no effect in either assay. Molecular modelling of HCII 1-75 correctly predicted those portions of the acidic extension that had been previously visualized in crystal structures, and suggested that an α-helix found between residues 26 and 36 stabilizes one found between residues 61-67. The latter region has been previously shown by deletion mutagenesis and crystallography to play a crucial role in the binding of HCII to thrombin exosite 1. Conclusions Assuming that the K D value for HCII 1-75 of 330-340 nM faithfully predicts that of this region in intact HCII, and that 1-75 binding to exosite 1 is GAG-dependent, our results support a model in which thrombin first binds to GAGs, followed by HCII addition to the ternary complex and release of HCII 1-75 for exosite 1 binding and serpin mechanism inhibition. They further suggest that, in isolated or transferred form, the entire HCII 1-75 region is required to ensure maximal binding of thrombin exosite 1.
    Type of Medium: Online Resource
    ISSN: 1471-2091
    URL: Article
    DOI: 10.1186/1471-2091-14-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
    detail.hit.zdb_id: 2041216-2
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Reduction of thrombus size in murine models of thrombosis following administration of recombinant α1-proteinase inhibitor mutant proteins
    Georg Thieme Verlag KG ; 2012
    In:  Thrombosis and Haemostasis Vol. 107, No. 05 ( 2012), p. 972-984
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 107, No. 05 ( 2012), p. 972-984
    Abstract: The variant serpin α1-PI M358R inhibits thrombin and other proteases such as activated protein C (APC) and factor XIa. We previously described recombinant proteins HAPI M358R (α1-PI M358R containing an N-terminal extension corresponding to residues 1–75 of heparin cofactor II) and HAPI RCL5 (HAPI M358R with F352-I356 and I360 substituted for the corresponding residues of antithrombin), with enhanced selectivity for thrombin over APC inhibition. We tested the hypotheses that these recombinant proteins would limit thrombosis in three mouse models, and that the HAPI chimeric proteins would be more effective than α1-PI M358R. Recombinant serpins were purified from Escherichia coli by nickel chelate and ion exchange affinity chromatography, and administered to mice intravenously. HAPI RCL5 reduced incorporation of radiolabelled fibrin(ogen) into thrombi in the ferric chloride-injured vena cava in a dose-dependent manner; HAPI M358R was less effective and α1-PI M358R was without effect. In a model of murine endotoxaemia, HAPI RCL5 was more effective than α1-PI M358R in reducing radiolabelled fibrin(ogen) deposition in heart and kidneys; immunohis-tochemistry of tissue sections showed lesser staining with anti-fibrin(ogen) antibodies with both treatments. In the ferric chloride-injured murine carotid artery, administration of both recombinant serpins was equally effective in lengthening the vessel’s time to occlusion. Our results show that the antithrombotic efficacy of the recombinant serpins correlates with their potency as thrombin inhibitors, since HAPI RCL5 inhibits thrombin, but not factors Xa, XIa, XIIa, or neutrophil elastase, more rapidly than α1-PI M358R.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH11-09-0604
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2012
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  • 9
    Online Resource
    Online Resource
    Molecular Cloning and Cell-Free Expression of Mouse Antithrombin III
    Georg Thieme Verlag KG ; 1992
    In:  Thrombosis and Haemostasis Vol. 68, No. 03 ( 1992), p. 291-296
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 68, No. 03 ( 1992), p. 291-296
    Abstract: The homology between antithrombin III (AT-III) of mouse, of man, and that of other species was investigated. Preliminary experiments showed that mouse AT-III inhibited human α-thrombin efficiently (second order rate constant [K 2nd] 5.8 × 103 M–1 s–1) as compared to human AT-III (K 2nd 6.7 × 103 M–1), but was not recognized on immunoblots by antibodies that recognized both human and rabbit AT-III. In order to compare AT-III from different species at the molecular level, a cDNA clone for murine AT-III was isolated from a λZAP mouse liver cDNA library on the basis of hybridization to a rabbit AT-III cDNA probe. The 1509 bp murine AT-III cDNA consists of a 1398 bp open reading frame, preceded by a 15 bp 5’ untranslated region, followed by a 75 bp 3’ untranslated region. The deduced primary protein structure consists of a 32 amino acid signal sequence, with a mature portion of 433 residues. Mature murine AT-III is 89% identical to its human counterpart, 86% identical to bovine AT-III, and 82% identical to that of the rabbit. Constructs lacking the nucleotides encoding the signal sequence were engineered and expressed in a cell-free system. The resulting 47 kDa non-glycosylated translation product was capable of being cleaved by human α-thrombin, of forming SDS-stable complexes with the protease, and of binding to immobilized heparin. Isolation of the murine AT-III cDNA will make feasible molecularly defined experiments with murine AT-III in the mouse system.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0038-1656367
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 1992
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  • 10
    Online Resource
    Online Resource
    Accelerated apoptotic death and in vivo turnover of erythrocytes in mice lacking functional mitogen- and stress-activated kinase MSK1/2
    Springer Science and Business Media LLC ; 2015
    In:  Scientific Reports Vol. 5, No. 1 ( 2015-11-27)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 5, No. 1 ( 2015-11-27)
    Abstract: The mitogen- and stress-activated kinase MSK1/2 plays a decisive role in apoptosis. In analogy to apoptosis of nucleated cells, suicidal erythrocyte death called eryptosis is characterized by cell shrinkage and cell membrane scrambling leading to phosphatidylserine (PS) externalization. Here, we explored whether MSK1/2 participates in the regulation of eryptosis. To this end, erythrocytes were isolated from mice lacking functional MSK1/2 ( msk −/− ) and corresponding wild-type mice ( msk +/+ ). Blood count, hematocrit, hemoglobin concentration and mean erythrocyte volume were similar in both msk −/− and msk +/+ mice, but reticulocyte count was significantly increased in msk −/− mice. Cell membrane PS exposure was similar in untreated msk −/− and msk +/+ erythrocytes, but was enhanced by pathophysiological cell stressors ex vivo such as hyperosmotic shock or energy depletion to significantly higher levels in msk −/− erythrocytes than in msk +/+ erythrocytes. Cell shrinkage following hyperosmotic shock and energy depletion, as well as hemolysis following decrease of extracellular osmolarity was more pronounced in msk −/− erythrocytes. The in vivo clearance of autologously-infused CFSE-labeled erythrocytes from circulating blood was faster in msk −/− mice. The spleens from msk −/− mice contained a significantly greater number of PS-exposing erythrocytes than spleens from msk +/+ mice. The present observations point to accelerated eryptosis and subsequent clearance of erythrocytes leading to enhanced erythrocyte turnover in MSK1/2-deficient mice.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/srep17316
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2015
    detail.hit.zdb_id: 2615211-3
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