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  1. Article ; Online: Doctors-in-Training and COVID-19 Misinformation on Social Media.

    Ma, Colleen Lok Kum / Soomro, Asim / Deng, Yue Yi

    Asia-Pacific journal of public health

    2021  Volume 33, Issue 8, Page(s) 961–963

    MeSH term(s) COVID-19 ; Communication ; Humans ; Physicians ; SARS-CoV-2 ; Social Media
    Language English
    Publishing date 2021-07-30
    Publishing country China
    Document type Journal Article
    ZDB-ID 1025444-4
    ISSN 1941-2479 ; 1010-5395
    ISSN (online) 1941-2479
    ISSN 1010-5395
    DOI 10.1177/10105395211032420
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2802: Show issues Location:
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  2. Article ; Online: The duplication mutation of Quebec platelet disorder dysregulates PLAU, but not C10orf55, selectively increasing production of normal PLAU transcripts by megakaryocytes but not granulocytes.

    Hayward, Catherine P M / Liang, Minggao / Tasneem, Subia / Soomro, Asim / Waye, John S / Paterson, Andrew D / Rivard, Georges E / Wilson, Michael D

    PloS one

    2017  Volume 12, Issue 3, Page(s) e0173991

    Abstract: Quebec Platelet disorder (QPD) is a unique bleeding disorder that markedly increases urokinase plasminogen activator (uPA) in megakaryocytes and platelets but not in plasma or urine. The cause is tandem duplication of a 78 kb region of chromosome 10 ... ...

    Abstract Quebec Platelet disorder (QPD) is a unique bleeding disorder that markedly increases urokinase plasminogen activator (uPA) in megakaryocytes and platelets but not in plasma or urine. The cause is tandem duplication of a 78 kb region of chromosome 10 containing PLAU (the uPA gene) and C10orf55, a gene of unknown function. QPD increases uPA in platelets and megakaryocytes >100 fold, far more than expected for a gene duplication. To investigate the tissue-specific effect that PLAU duplication has on gene expression and transcript structure in QPD, we tested if QPD leads to: 1) overexpression of normal or unique PLAU transcripts; 2) increased uPA in leukocytes; 3) altered levels of C10orf55 mRNA and/or protein in megakaryocytes and leukocytes; and 4) global changes in megakaryocyte gene expression. Primary cells and cultured megakaryocytes from donors were prepared for quantitative reverse polymerase chain reaction analyses, RNA-seq and protein expression analyses. Rapidly isolated blood leukocytes from QPD subjects showed only a 3.9 fold increase in PLAU transcript levels, in keeping with the normal to minimally increased uPA in affinity purified, QPD leukocytes. All subjects had more uPA in granulocytes than monocytes and minimal uPA in lymphocytes. QPD leukocytes expressed PLAU alleles in proportions consistent with an extra copy of PLAU on the disease chromosome, unlike QPD megakaryocytes. QPD PLAU transcripts were consistent with reference gene models, with a much higher proportion of reads originating from the disease chromosome in megakaryocytes than granulocytes. QPD and control megakaryocytes contained minimal reads for C10orf55, and C10orf55 protein was not increased in QPD megakaryocytes or platelets. Finally, our QPD megakaryocyte transcriptome analysis revealed a global down regulation of the interferon type 1 pathway. We suggest that the low endogenous levels of uPA in blood are actively regulated, and that the regulatory mechanisms are disrupted in QPD in a megakaryocyte-specific manner.
    MeSH term(s) Factor V Deficiency/genetics ; Gene Duplication ; Granulocytes/metabolism ; Humans ; Megakaryocytes/metabolism ; Mutation ; Open Reading Frames ; RNA, Messenger/biosynthesis ; Reverse Transcriptase Polymerase Chain Reaction ; Urokinase-Type Plasminogen Activator/genetics
    Chemical Substances RNA, Messenger ; Urokinase-Type Plasminogen Activator (EC 3.4.21.73)
    Language English
    Publishing date 2017-03-16
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0173991
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Enhancer-gene rewiring in the pathogenesis of Quebec platelet disorder.

    Liang, Minggao / Soomro, Asim / Tasneem, Subia / Abatti, Luis E / Alizada, Azad / Yuan, Xuefei / Uusküla-Reimand, Liis / Antounians, Lina / Alvi, Sana Akhtar / Paterson, Andrew D / Rivard, Georges-Étienne / Scott, Ian C / Mitchell, Jennifer A / Hayward, Catherine P M / Wilson, Michael D

    Blood

    2020  Volume 136, Issue 23, Page(s) 2679–2690

    Abstract: Quebec platelet disorder (QPD) is an autosomal dominant bleeding disorder with a unique, platelet-dependent, gain-of-function defect in fibrinolysis, without systemic fibrinolysis. The hallmark feature of QPD is a >100-fold overexpression of PLAU, ... ...

    Abstract Quebec platelet disorder (QPD) is an autosomal dominant bleeding disorder with a unique, platelet-dependent, gain-of-function defect in fibrinolysis, without systemic fibrinolysis. The hallmark feature of QPD is a >100-fold overexpression of PLAU, specifically in megakaryocytes. This overexpression leads to a >100-fold increase in platelet stores of urokinase plasminogen activator (PLAU/uPA); subsequent plasmin-mediated degradation of diverse α-granule proteins; and platelet-dependent, accelerated fibrinolysis. The causative mutation is a 78-kb tandem duplication of PLAU. How this duplication causes megakaryocyte-specific PLAU overexpression is unknown. To investigate the mechanism that causes QPD, we used epigenomic profiling, comparative genomics, and chromatin conformation capture approaches to study PLAU regulation in cultured megakaryocytes from participants with QPD and unaffected controls. QPD duplication led to ectopic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topologically associating domain (TAD). Our results support a unique disease mechanism whereby the reorganization of sub-TAD genome architecture results in a dramatic, cell-type-specific blood disorder phenotype.
    MeSH term(s) Animals ; Enhancer Elements, Genetic ; Factor V Deficiency/genetics ; Factor V Deficiency/metabolism ; Factor V Deficiency/pathology ; Female ; Gene Duplication ; Gene Expression Regulation ; Humans ; Megakaryocytes/metabolism ; Megakaryocytes/pathology ; Membrane Proteins/biosynthesis ; Membrane Proteins/genetics ; Zebrafish
    Chemical Substances Membrane Proteins ; PLAU protein, human
    Language English
    Publishing date 2020-07-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020005394
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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