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1.
  • Widell, A., et al. (författare)
  • At least three hepatitis C virus strains implicated in Swedish and Danish patients with intravenous immunoglobulin-associated hepatitis C
  • 1997
  • Ingår i: Transfusion. - : Wiley-Blackwell. - 0041-1132 .- 1537-2995. - 0041-1132 (Print) 0041-1132 (Linking) ; 37:3, s. 313-20
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Three reported Swedish cases of hepatitis C in patients receiving an intravenous immunoglobulin (Gammagard, Baxter Healthcare, Deerfield, IL) were among the first to bring to light a worldwide outbreak of hepatitis C associated with non-solvent/detergent (SD)-treated Gammagard. In February 1994, all implicated batches of Gammagard were recalled and exposed patients traced. STUDY DESIGN AND METHODS: Sera from all identified and hepatitis C-viremic Swedish and Danish patients (n = 14) exposed to the implicated batches underwent hepatitis C virus genotyping and sequencing of the core region and hypervariable region 1 of E2. Genomic amplification was also done on 15 non-SD-treated batches of Gammagard. RESULTS: Twelve patients were infected with subtype 1a and surprisingly, two with subtype 2b. Analysis of the core region showed identical sequences in four patients and the only consistently positive batch. Five patients shared another sequence, whereas three other subtype 1a patients each manifested unique sequences. The two subtype 2b isolates were identical. Genomic fingerprinting of the hypervariable region confirmed identity within each group with great stringency. Amplification with isolate-specific primers showed mixed infection in one patient whose exposure was confined to a single batch. CONCLUSION: The few batches implicated presumably were contaminated with several strains.
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  • Wester, Elisabet S, et al. (författare)
  • Genetic basis of the K(0) phenotype in the Swedish population.
  • 2005
  • Ingår i: Transfusion. - 0041-1132 .- 1537-2995. ; 45:4, s. 545-9
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The absence of all Kell blood group antigens (K(0) phenotype) is very rare. K(0) persons, however, can produce clinically significant anti-Ku (K5) after transfusion and/or pregnancy and require K(0) blood for transfusion. Ten alleles giving rise to the K(0) phenotype have been reported: different populations were studied although none from Scandinavia. STUDY DESIGN AND METHODS: Three K(0) samples were identified by blood banks in Sweden (Uppsala, Umeå, and Linköping) during a 20-year period. Kell antigen typing was performed with standard serologic techniques by the respective blood banks and K(0) status was confirmed by the International Blood Group Reference Laboratory in Bristol, England. Polymerase chain reaction and DNA sequencing of the KEL coding region (exons 1-19) was performed on genomic DNA. RESULTS: The Uppsala K(0) was homozygous for a 1540C>T substitution in exon 13, leading to an immediate stop codon. The Umeå K(0) was homozygous for 1023delG in exon 8 that results in a frameshift and a premature stop codon in exon 9. In the Linköping K(0), a previously reported mutation g>a at +1 of intron 3 was found. CONCLUSION: Two novel and one previously reported null alleles at the KEL locus are described. The identified nonsense mutations abolish expression of the Kell glycoprotein and are thus responsible for the K(0) phenotype in these Swedish families.
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  • Aslam, Rukhsana, et al. (författare)
  • Platelet and red blood cell phagocytosis kinetics are differentially controlled by phosphatase activity within mononuclear cells
  • Ingår i: Transfusion. - : Wiley-Blackwell. - 0041-1132. ; 47:11, s. 2161-2168
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Anti-D treatment is effective in increasing platelet (PLT) counts in patients with autoimmune thrombocytopenic purpura (AITP); however, the exact mechanism of action is unknown. Previous results have suggested that anti-D-coated red blood cells (RBCs) affect reticuloendothelial system phagocytosis by stimulating agents (e.g., reactive oxygen species) that alter signaling pathways within the phagocyte. To address this, a flow cytometric assay was used to compare the kinetics and signaling pathways responsible for opsonized PLT and RBC phagocytosis. STUDY DESIGN AND METHODS: Human RBCs or PLTs were labeled with the fluorescent dye CM-Green, opsonized with Rh immune globulin or anti-MHC, respectively, and incubated with THP-1 monocytes with or without signal transduction inhibitors and intracellular fluorescence was analyzed. RESULTS: Compared with opsonized PLTs, phagocytosis of opsonized RBCs was significantly slower (p < 0.0001) and, within 2 hours, induced a state of phagocytic refractoriness; resting the mononuclear cells (MNCs) for up to 24 hours did not rescue their ability to further mediate PLT phagocytosis. Inhibitors of phosphatidylinositol 3-kinase (wortmannin, LY294002, myricetin, and quercetin), protein kinase C (staurosporine), and Syk kinase (piceatannol) inhibited both opsonized RBC and opsonized PLT phagocytosis. In contrast, opsonized RBC phagocytosis was significantly (p < 0.0001) enhanced by the tyrosine phosphatase inhibitor phenyl arsine oxide, whereas PLT phagocytosis was significantly reduced (p < 0.0001). Of interest, phosphatase inhibition during opsonized RBC phagocytosis induced a longer (48 hr) phagocytic refractoriness period in the MNCs. CONCLUSION: These results suggest that the early kinetics and signaling events related to phosphatase activity regulate how mononuclear phagocytes engulf opsonized RBCs and induce phagocytic refractoriness for further PLT phagocytosis.
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  • Barro, Lassina, et al. (författare)
  • A double-virally-inactivated (Intercept-solvent/detergent) human platelet lysate for in vitro expansion of human mesenchymal stromal cells
  • 2019
  • Ingår i: Transfusion. - : John Wiley & Sons. - 0041-1132 .- 1537-2995. ; 59:6, s. 2061-2073
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND Pooled human platelet lysate (HPL) can replace fetal bovine serum (FBS) as xeno-free supplement for ex vivo expansion of mesenchymal stromal cells (MSCs). We evaluate here whether a double-virally-inactivated HPL (DVI-HPL) prepared from expired Intercept-treated platelet concentrates (PCs) and treated by solvent/detergent (S/D) can be used for MSC expansion. STUDY DESIGN AND METHODS Expired Intercept-treated PCs in 65% platelet (PLT) additive solution were pooled and subjected to a 1% tri-n-butyl phosphate/1% Triton X-45 treatment followed by soybean oil, hydrophobic interaction chromatography purification, and sterile filtration. Bone marrow-derived MSCs (BM-MSCs) were expanded for four passages in growth medium containing 10% DVI-HPL, I-HPL (from Intercept-PC only), untreated HPL, and FBS. MSC morphology, doubling time, immunophenotype, immunosuppressive activity, and differentiation capacity were compared. RESULTS Expanded cells had typical spindle morphology and showed higher viability in all HPL conditions than in FBS. The DVI-HPL and FBS-expanded cells were morphologically larger than in I-HPL and HPL supplements. The cumulative population doubling was lower using DVI-HPL than with HPL and I-HPL, but significantly higher than using FBS. Immunophenotype was not affected by the supplements used. Immunosuppressive activity was maintained with all supplements. Differentiation capacity into chondrocytes and osteocytes was more effective in DVI-HPL but less toward adipocytes compared to other supplements. CONCLUSIONS Human PLT lysate made from Intercept-PCs subjected to S/D treatment may be an alternative to untreated HPL and to I-HPL for BM-MSC expansion. This finding reinforces the potential of HPL as a virally safe alternative to FBS for clinical grade MSC expansion protocols.
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8.
  • Berglund, David, et al. (författare)
  • Green plasma
  • 2015
  • Ingår i: Transfusion. - 0041-1132 .- 1537-2995. ; 55:2, s. 245-245
  • Tidskriftsartikel (övrigt vetenskapligt)
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