Bent Lind
University of Copenhagen
35 Papers
98 Citations
Bent Lind is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 11, co-authored 24 publications. Previous affiliations of Bent Lind include Hvidovre Hospital.
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Papers
Splice site mutation in the human protein C gene associated with venous thrombosis: demonstration of exon skipping by ectopic transcript analysis.
TL;DR: Analysis of human liver protein C mRNA indicated that the ectopic lymphocyte mRNA was qualitatively representative for the tissue-specific mRNA, which agrees with the observation that the mutation results in a type 1 protein C deficiency.
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A novel missense mutation in the human plasmin inhibitor (alpha2-antiplasmin) gene associated with a bleeding tendency.
Bent Lind,Sixtus Thorsen +1 more
TL;DR: Heterozygosity for a G’→ A mutation converting Val384(GTG) to Met(ATG) associated with plasmin inhibitor (alpha2‐antiplasmin) deficiency was identified in three family members with bleeding tendency and crossed immunoelectrophoresis of plasma from the proband showed a normal pattern.
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Prevalence and clinical significance of neutropenia discovered in routine complete blood cell counts: a longitudinal study
Christen Lykkegaard Andersen,Christen Lykkegaard Andersen,D. Tesfa,Volkert Siersma,Håkon Sandholdt,Hans Carl Hasselbalch,Ole Weis Bjerrum,Peter Felding,Bent Lind,Niels de Fine Olivarius,Jan Palmblad +10 more
TL;DR: Neutropenia, defined as an absolute blood neutrophil count (ANC) <1.5 G L−1, may accompany a variety of diseases and is poorly understood.
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A specific immunologic assay for functional plasminogen activator inhibitor 1 in plasma--standardized measurements of the inhibitor and related parameters in patients with venous thromboembolic disease.
TL;DR: It was found that the patients had a decreased fibrinolytic capacity and this could be ascribed to high plasma levels of PAI-1, and no significant difference could be demonstrated between the patients with a thrombotic tendency and the normal subjects.
22
Characterization and structural impact of five novel PROS1 mutations in eleven protein S-deficient families.
Bente Damm Andersen,Marie Luise Bisgaard,Bent Lind,Malou Philips,Bruno O. Villoutreix,Sixtus Thorsen +5 more
TL;DR: The mutations reported here are most likely the cause of the protein S deficiency and are compatible with defective protein folding/unstable molecules, impaired secretion and intracellular degradation of mutated protein, which appear to be the major molecular disease mechanisms for missense mutations and certain other mutations found in genetic disorders.
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