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Träfflista för sökning "L773:0957 5235 OR L773:1473 5733 srt2:(2020-2022)"

Sökning: L773:0957 5235 OR L773:1473 5733 > (2020-2022)

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1.
  • Srinivasa, Chandramma, et al. (författare)
  • Caesalpinia cristacoat extract protects red blood cell from sodium nitrite-induced oxidative stress and exhibits antiplatelet activity
  • 2020
  • Ingår i: Blood Coagulation and Fibrinolysis. - : LIPPINCOTT WILLIAMS & WILKINS. - 0957-5235 .- 1473-5733. ; 31:5, s. 293-302
  • Tidskriftsartikel (refereegranskat)abstract
    • To understand the RBC protecting efficiency and antiplatelet activity of methanolic extract ofCaesalpinia cristacoat (MECCC). RBC-protecting activity of MECCC was evaluated using assays, such as DPPH, level of lipid peroxidation, protein carbonyl content, superoxide dismutase and catalase as a marker of oxidative stress whereas, platelet aggregation inhibition was performed using human platelet-rich plasma (PRP). MECCC showed about 76% of DPPH-scavenging activity, with an IC(50)value of 71.89 mu g/ml. The MECCC reduced the level of lipid peroxidation and protein carboxylation in RBC caused by NaNO(2)in a dose-dependent manner. In addition, MECCC normalized the levels of superoxide dismutase (SOD) and catalase (CAT) in oxidative stress-induced RBC in a dose-dependent manner. This suggested the protective effect of MECCC on RBC against oxidative stress. Furthermore, MECCC also exhibited mild antiplatelet activity by inhibiting both ADP and epinephrine agonists that induced platelet aggregation. The noticed inhibition percentage was found to be 28 and 23%, respectively at the concentration of 150 mu g. Interestingly, MECCC did not hydrolyse the RBC suggesting its nontoxic properties. MECCC possesses protective effect of RBC against NaNO2(10 mmol/l) induce oxidative stress and inhibits platelet aggregation.
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2.
  • Fager Ferrari, Marcus, et al. (författare)
  • A rare heterozygous variant in FGB (Fibrinogen Merivale) causing hypofibrinogenemia in a Swedish family
  • 2020
  • Ingår i: Blood Coagulation and Fibrinolysis. - 1473-5733. ; 31:7, s. 481-484
  • Tidskriftsartikel (refereegranskat)abstract
    • Fibrinogen is essential for normal hemostasis. Congenital fibrinogen disorders (afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia and hypodysfibrinogenemia), caused by pathogenic variants in the genes FGA, FGB and FGG, have the potential of causing bleeding diathesis and/or thrombotic events of variable severity. We describe a case of familial hypofibrinogenemia in a Swedish family. The proband is a 27-year-old woman, with a history of significant bleeding diathesis. She was diagnosed with moderate hypofibrinogenemia (0.8 g/l), and genetic screening identified a rare heterozygous missense variant in FGB (c.854G>A, p.Arg285His) (Fibrinogen Merivale) previously described in a New Zealand European family with symptomatic hypofibrinogenemia. The father, sister and brother of the proband also harbored the FGB variant, segregating with hypofibrinogenemia (0.9-1.2 g/l). The proband showed a more severe bleeding phenotype compared with her other hypofibrinogenemic family members; this was attributed to a concomitant platelet dysfunction, also present in her normofibrinogenemic mother.
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  • Guné, Henrik, et al. (författare)
  • Impact of ABO blood group on bleeding complications after surgery for acute type A aortic dissection
  • 2021
  • Ingår i: Blood Coagulation and Fibrinolysis. - 1473-5733. ; 32:4, s. 253-258
  • Tidskriftsartikel (refereegranskat)abstract
    • Excessive bleeding is a serious complication associated with impaired survival after surgery for acute type A aortic dissection (ATAAD). Different ABO blood groups are associated with variable levels of circulating von Willebrand factor and therefore potentially altered risks of surgical haemorrhage. The current study aimed to assess the impact of blood group on bleeding complications after ATAAD surgery. This was a retrospective cohort study including 336 patients surgically treated for ATAAD between January 2004 and January 2019. Patients with blood group O were compared with non-O patients. In total, 152 blood group O patients were compared with 184 non-O patients. There were no differences in rates of massive bleeding (27.0 vs. 25.5%, P = 0.767) or re-exploration for bleeding (16.4 vs. 13.0%, P = 0.379) in blood group O and non-O patients, respectively. Median chest tube output 12 h after surgery was 520 ml (350-815 ml) in blood group O and 490 ml (278-703 ml) in non-O patients (P = 0.229). Blood group O patients received more fibrinogen concentrate (6.1 ± 4.0 vs. 4.9 ± 3.3 g, P = 0.023) but administered units of packed red blood cells [5 (2-8) vs. 4 (2-9) U, P = 0.736], platelets [4 (2-4) vs. 3 (2-5) U, P = 0.521] or plasma [4 (1-7) vs. 4 (0-7) U, P = 0.562] were similar. This study could not demonstrate any association between blood group and bleeding after surgery for ATAAD. It cannot be ruled out that potential differences were levelled out by blood group O patients receiving significantly more fibrinogen concentrate.
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