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  1. Book: Translational cardiometabolic genomic medicine

    Rodriguez-Oquendo, Annabelle

    2015  

    Author's details ed. by Annabelle Rodriguez-Oquendo
    Keywords Genomics
    Subject code 572.86
    Language English
    Size XII, 340 S. : Ill., graph. Darst., 23 cm
    Publisher Elsevier Acad. Press
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT018770707
    ISBN 978-0-12-799961-6 ; 0-12-799961-2
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2015 A 3376 available for loan (reading room) Lesesaal EG

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  2. Book: Translational cardiometabolic genomic medicine

    Rodriguez-Oquendo, Annabelle

    2016  

    Author's details edited by Annabelle Rodriguez-Oquendo
    MeSH term(s) Genetics, Medical ; Genomics ; Cardiovascular Diseases/genetics ; Metabolic Diseases/genetics
    Language English
    Dates of publication 2016-2016
    Size xii, 340 pages :, illustrations ;, 24 cm
    Document type Book
    ISBN 9780127999616 ; 0127999612 ; 9780128004746 ; 0128004746
    Database Catalogue of the US National Library of Medicine (NLM)

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  3. Book ; Online: Translational Cardiometabolic Genomic Medicine

    Rodriguez-Oquendo, Annabelle

    2015  

    Abstract: Translational Cardiometabolic Genomic Medicine,edited by Dr. Annabelle Rodriguez-Oquendo, is an important resource to postgraduate (medical, dental and graduate) students, postdoctoral fellows, basic scientists, and physician scientists seeking to ... ...

    Abstract Translational Cardiometabolic Genomic Medicine,edited by Dr. Annabelle Rodriguez-Oquendo, is an important resource to postgraduate (medical, dental and graduate) students, postdoctoral fellows, basic scientists, and physician scientists seeking to understand and expand their knowledge base in the field of genomic medicine as it is applied to cardiometabolic diseases. This handbook integrates cutting-edge experimental approaches such as chromatin immunoprecipitation paired end tagging (CHIA-PET), to population studies such as the Multi-Ethnic Study of Atherosclerosis. It encompasses a range of book chapters that highlight bioinformatic approaches to better understanding functionality of the noncoding regions of the human genome to the use of molecular diagnostic testing in predicting increased risk of cardiovascular diseases. Where applicable, this reference also includes chapters related to therapeutic options specifically aligned to molecular targets.Provides comprehensive research on translational genomic medicine Explains state-of-the-art genome editing for stem cells and mouse models with significant relevance to human cardiometabolic diseaseIncludes discussions on the functional effects of single nucleotide polymorphisms and cardiometabolic diseases, stratified by sex and raceEncompasses a range of book chapters that highlight bioinformatic approaches to better understanding functionality of the noncoding regions of the human genome
    Language English
    Size Online-Ressource
    Edition 1. Aufl.
    Publisher Elsevier Reference Monographs
    Publishing place s.l.
    Document type Book ; Online
    Note Description based upon print version of record
    ISBN 0127999612 ; 9780127999616
    Database Former special subject collection: coastal and deep sea fishing

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  4. Article ; Online: Splice factor polypyrimidine tract-binding protein 1 (Ptbp1) primes endothelial inflammation in atherogenic disturbed flow conditions.

    Hensel, Jessica A / Nicholas, Sarah-Anne E / Kimble, Amy L / Nagpal, Arjun S / Omar, Omar M F / Tyburski, Jordan D / Jellison, Evan R / Ménoret, Antoine / Ozawa, Manabu / Rodriguez-Oquendo, Annabelle / Vella, Anthony T / Murphy, Patrick A

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Volume 119, Issue 30, Page(s) e2122227119

    Abstract: NF-κB-mediated endothelial activation drives leukocyte recruitment and atherosclerosis, in part through adhesion molecules Icam1 and Vcam1. The endothelium is primed for cytokine activation of NF-κB by exposure to low and disturbed blood flow (LDF)but ... ...

    Abstract NF-κB-mediated endothelial activation drives leukocyte recruitment and atherosclerosis, in part through adhesion molecules Icam1 and Vcam1. The endothelium is primed for cytokine activation of NF-κB by exposure to low and disturbed blood flow (LDF)but the molecular underpinnings are not fully understood. In an experimental in vivo model of LDF, platelets were required for the increased expression of several RNA-binding splice factors, including polypyrimidine tract binding protein (Ptbp1). This was coordinated with changes in RNA splicing in the NF-κB pathway in primed cells, leading us to examine splice factors as mediators of priming. Using Icam1 and Vcam1 induction by tumor necrosis factor (TNF)-α stimulation as a readout, we performed a CRISPR Cas9 knockout screen and identified a requirement for Ptbp1 in priming. Deletion of Ptbp1 had no effect on cell growth or response to apoptotic stimuli, but reversed LDF splicing patterns and inhibited NF-κB nuclear translocation and transcriptional activation of downstream targets, including Icam1 and Vcam1. In human coronary arteries, elevated PTBP1 correlates with expression of TNF pathway genes and plaque. In vivo, endothelial-specific deletion of Ptbp1 reduced Icam1 expression and myeloid cell infiltration at regions of LDF in atherosclerotic mice, limiting atherosclerosis. This may be mediated, in part, by allowing inclusion of a conserved alternative exon in Ripk1 leading to a reduction in Ripk1 protein. Our data show that Ptbp1, which is induced in a subset of the endothelium by platelet recruitment at regions of LDF, is required for priming of the endothelium for subsequent NF-κB activation, myeloid cell recruitment and atherosclerosis.
    MeSH term(s) Alternative Splicing ; Animals ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Endothelium/metabolism ; Heterogeneous-Nuclear Ribonucleoproteins/genetics ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Mice ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Polypyrimidine Tract-Binding Protein/genetics ; Polypyrimidine Tract-Binding Protein/metabolism
    Chemical Substances Heterogeneous-Nuclear Ribonucleoproteins ; NF-kappa B ; PTBP1 protein, human ; Ptbp1 protein, mouse ; Polypyrimidine Tract-Binding Protein (139076-35-0)
    Language English
    Publishing date 2022-07-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2122227119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Understanding how combinatorial targeting of TLRs and TNFR family costimulatory members promote enhanced T cell responses.

    Shinde, Paurvi / Bharat, Vinita / Rodriguez-Oquendo, Annabelle / Zhou, Beiyan / Vella, Anthony T

    Expert opinion on biological therapy

    2018  Volume 18, Issue 10, Page(s) 1073–1083

    Abstract: Introduction: Due to the ability of pathogen-associated molecular patters and tumor necrosis factor receptor (TNFR) family costimulatory agonists to boost T cell responses, studies have combined Toll-like receptor (TLR) ligands with TNFR family ... ...

    Abstract Introduction: Due to the ability of pathogen-associated molecular patters and tumor necrosis factor receptor (TNFR) family costimulatory agonists to boost T cell responses, studies have combined Toll-like receptor (TLR) ligands with TNFR family costimulatory receptor agonists to induce impressive and long-lasting T cell responses. Although some studies have determined how these combinatorial vaccines promote enhanced T cell responses, much remains unknown about the mechanism used by these combinations to promote synergistic T cell responses - especially in settings of infectious diseases or cancer.
    Areas covered: In this review, we look in detail at the signaling pathways induced by combinatorial targeting of TLR and TNFR family costimulatory members that help them promote synergistic T cell responses. Understanding this can greatly aid the development of novel vaccine regimens that promote cellular immune responses, which is essential for treating certain infectious diseases and cancer.
    Expert opinion: Vaccines against some infectious diseases as well as therapeutic cancer vaccines require cellular immunity. Therefore, we evaluate here how signaling pathways induced by TLR ligand and costimulatory agonist combinations promote enhanced T cell responses during immunization with model antigens, viral pathogens, or tumor antigens. Once pathways that drive these combinatorial vaccines to boost T cell activation are identified, they can be incorporated in vaccines designed to target pathogens or cancer.
    MeSH term(s) Adjuvants, Immunologic/pharmacology ; Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cancer Vaccines/pharmacology ; Combined Modality Therapy ; Drug Delivery Systems/methods ; Humans ; Immunity, Cellular/drug effects ; Lymphocyte Activation/drug effects ; Receptors, Tumor Necrosis Factor/antagonists & inhibitors ; Receptors, Tumor Necrosis Factor/immunology ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/physiology ; Toll-Like Receptors/antagonists & inhibitors ; Toll-Like Receptors/immunology
    Chemical Substances Adjuvants, Immunologic ; Cancer Vaccines ; Receptors, Tumor Necrosis Factor ; Toll-Like Receptors
    Language English
    Publishing date 2018-09-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2052501-1
    ISSN 1744-7682 ; 1471-2598
    ISSN (online) 1744-7682
    ISSN 1471-2598
    DOI 10.1080/14712598.2018.1518422
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    Zs.A 6094: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: AtheroSpectrum Reveals Novel Macrophage Foam Cell Gene Signatures Associated With Atherosclerotic Cardiovascular Disease Risk.

    Li, Chuan / Qu, Lili / Matz, Alyssa J / Murphy, Patrick A / Liu, Yongmei / Manichaikul, Ani W / Aguiar, Derek / Rich, Stephen S / Herrington, David M / Vu, David / Johnson, W Craig / Rotter, Jerome I / Post, Wendy S / Vella, Anthony T / Rodriguez-Oquendo, Annabelle / Zhou, Beiyan

    Circulation

    2021  Volume 145, Issue 3, Page(s) 206–218

    Abstract: Background: Whereas several interventions can effectively lower lipid levels in people at risk for atherosclerotic cardiovascular disease (ASCVD), cardiovascular event risks remain, suggesting an unmet medical need to identify factors contributing to ... ...

    Abstract Background: Whereas several interventions can effectively lower lipid levels in people at risk for atherosclerotic cardiovascular disease (ASCVD), cardiovascular event risks remain, suggesting an unmet medical need to identify factors contributing to cardiovascular event risk. Monocytes and macrophages play central roles in atherosclerosis, but studies have yet to provide a detailed view of macrophage populations involved in increased ASCVD risk.
    Methods: A novel macrophage foaming analytics tool, AtheroSpectrum, was developed using 2 quantitative indices depicting lipid metabolism and the inflammatory status of macrophages. A machine learning algorithm was developed to analyze gene expression patterns in the peripheral monocyte transcriptome of MESA participants (Multi-Ethnic Study of Atherosclerosis; set 1; n=911). A list of 30 genes was generated and integrated with traditional risk factors to create an ASCVD risk prediction model (30-gene cardiovascular disease risk score [CR-30]), which was subsequently validated in the remaining MESA participants (set 2; n=228); performance of CR-30 was also tested in 2 independent human atherosclerotic tissue transcriptome data sets (GTEx [Genotype-Tissue Expression] and GSE43292).
    Results: Using single-cell transcriptomic profiles (GSE97310, GSE116240, GSE97941, and FR-FCM-Z23S), AtheroSpectrum detected 2 distinct programs in plaque macrophages-homeostatic foaming and inflammatory pathogenic foaming-the latter of which was positively associated with severity of atherosclerosis in multiple studies. A pool of 2209 pathogenic foaming genes was extracted and screened to select a subset of 30 genes correlated with cardiovascular event in MESA set 1. A cardiovascular disease risk score model (CR-30) was then developed by incorporating this gene set with traditional variables sensitive to cardiovascular event in MESA set 1 after cross-validation generalizability analysis. The performance of CR-30 was then tested in MESA set 2 (
    Conclusions: Our novel computational program (AtheroSpectrum) identified a specific gene expression profile associated with inflammatory macrophage foam cells. A subset of 30 genes expressed in circulating monocytes jointly contributed to prediction of symptomatic atherosclerotic vascular disease. Incorporating a pathogenic foaming gene set with known risk factors can significantly strengthen the power to predict ASCVD risk. Our programs may facilitate both mechanistic investigations and development of therapeutic and prognostic strategies for ASCVD risk.
    MeSH term(s) Aged ; Aged, 80 and over ; Atherosclerosis/etiology ; Atherosclerosis/genetics ; Atherosclerosis/therapy ; Cardiovascular Diseases/complications ; Cardiovascular Diseases/therapy ; Coronary Artery Disease/complications ; Coronary Artery Disease/genetics ; Coronary Artery Disease/therapy ; Female ; Foam Cells/cytology ; Humans ; Macrophages/cytology ; Male ; Middle Aged ; Plaque, Atherosclerotic/complications ; Plaque, Atherosclerotic/genetics ; Plaque, Atherosclerotic/therapy ; ROC Curve ; Risk ; Vascular Calcification/complications ; Vascular Calcification/genetics ; Vascular Calcification/therapy
    Language English
    Publishing date 2021-12-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.121.054285
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.60: Show issues Location:
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