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  1. Article ; Online: Real-World Effectiveness of Fluticasone Furoate/Umeclidinium/Vilanterol Once-Daily Single-Inhaler Triple Therapy for Symptomatic COPD: The ELLITHE Non-Interventional Trial.

    Beeh, Kai-Michael / Scheithe, Karl / Schmutzler, Heike / Krüger, Saskia

    International journal of chronic obstructive pulmonary disease

    2024  Volume 19, Page(s) 205–216

    Abstract: Purpose: Real-life effectiveness data on once-daily single-inhaler triple therapy (odSITT) with the inhaled corticosteroid fluticasone furoate (FF), the long-acting muscarinic antagonist umeclidinium (UMEC), and the long-acting β: Patients and methods! ...

    Abstract Purpose: Real-life effectiveness data on once-daily single-inhaler triple therapy (odSITT) with the inhaled corticosteroid fluticasone furoate (FF), the long-acting muscarinic antagonist umeclidinium (UMEC), and the long-acting β
    Patients and methods: ELLITHE was a single-country (Germany), multicenter, open-label, non-interventional effectiveness study between 2020 and 2022, evaluating the effect of treatment initiation with FF/UMEC/VI 100/62.5/25 µg once-daily via the ELLIPTA inhaler on improvements in clinical outcomes versus baseline in COPD patients. The primary endpoint was the change in the total COPD Assessment Test (CAT) score between baseline and month 12. Key secondary endpoints included change in CAT score over time, occurrence of exacerbations until month 12, changes in forced expiratory volume in one second (FEV
    Results: Nine hundred and six patients were included (age 66.6 years, 55.6% male, mean FEV
    Conclusion: In usual care, treatment with odSITT resulted in significant and clinically relevant improvements of CAT score and FEV
    MeSH term(s) Humans ; Male ; Aged ; Female ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Fluticasone ; Nebulizers and Vaporizers ; Androstadienes ; Benzyl Alcohols ; Chlorobenzenes ; Quinuclidines
    Chemical Substances fluticasone furoate (JS86977WNV) ; GSK573719 ; vilanterol (028LZY775B) ; Fluticasone (CUT2W21N7U) ; Androstadienes ; Benzyl Alcohols ; Chlorobenzenes ; Quinuclidines
    Language English
    Publishing date 2024-01-17
    Publishing country New Zealand
    Document type Multicenter Study ; Journal Article
    ZDB-ID 2212419-6
    ISSN 1178-2005 ; 1176-9106
    ISSN (online) 1178-2005
    ISSN 1176-9106
    DOI 10.2147/COPD.S427770
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Matrix metalloproteinases in coronary artery disease and myocardial infarction.

    Bräuninger, Hanna / Krüger, Saskia / Bacmeister, Lucas / Nyström, Alexander / Eyerich, Kilian / Westermann, Dirk / Lindner, Diana

    Basic research in cardiology

    2023  Volume 118, Issue 1, Page(s) 18

    Abstract: Cardiovascular diseases (CVDs) remain the leading cause of death worldwide. Most cardiovascular deaths are caused by ischaemic heart diseases such as myocardial infarction (MI). Hereby atherosclerosis in the coronary arteries often precedes disease ... ...

    Abstract Cardiovascular diseases (CVDs) remain the leading cause of death worldwide. Most cardiovascular deaths are caused by ischaemic heart diseases such as myocardial infarction (MI). Hereby atherosclerosis in the coronary arteries often precedes disease manifestation. Since tissue remodelling plays an important role in the development and progression of atherosclerosis as well as in outcome after MI, regulation of matrix metalloproteinases (MMPs) as the major ECM-degrading enzymes with diverse other functions is crucial. Here, we provide an overview of the expression profiles of MMPs in coronary artery and left ventricular tissue using publicly available data from whole tissue to single-cell resolution. To approach an association between MMP expression and the development and outcome of CVDs, we further review studies investigating polymorphisms in MMP genes since polymorphisms are known to have an impact on gene expression. This review therefore aims to shed light on the role of MMPs in atherosclerosis and MI by summarizing current knowledge from publically available datasets, human studies, and analyses of polymorphisms up to preclinical and clinical trials of pharmacological MMP inhibition.
    MeSH term(s) Humans ; Coronary Artery Disease/genetics ; Myocardial Infarction/genetics ; Myocardial Ischemia ; Atherosclerosis ; Matrix Metalloproteinases
    Chemical Substances Matrix Metalloproteinases (EC 3.4.24.-)
    Language English
    Publishing date 2023-05-09
    Publishing country Germany
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-023-00987-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.30: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  3. Book ; Thesis: Hormonelle und metabolische Reaktionen auf anaerobe Belastung bei Patienten mit angeborenem klassischem adrenogenitalem Syndrom

    Krüger-Lassen, Saskia Nadine

    2007  

    Author's details vorgelegt von Saskia Nadine Krüger-Lassen
    Language German
    Size IV, 59 S. : graph. Darst.
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Kiel, Univ., Diss., 2007
    HBZ-ID HT015121604
    Database Catalogue ZB MED Medicine, Health

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    2007 D 716 order for loan Magazin

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  4. Article ; Online: High concentrations of vascular endothelial growth factor reduce stretch-induced apoptosis of alveolar type II cells.

    Kuhn, Hartmut / Krüger, Saskia / Hammerschmidt, Stefan / Wirtz, Hubert

    Respirology (Carlton, Vic.)

    2010  Volume 15, Issue 2, Page(s) 343–348

    Abstract: Unlabelled: Vascular endothelial growth factor (VEGF) has protective as well as injurious effects in ARDS/acute lung injury. The influence of VEGF was investigated in a model of stretch-induced apoptosis. High-amplitude mechanical stretch induced the ... ...

    Abstract Unlabelled: Vascular endothelial growth factor (VEGF) has protective as well as injurious effects in ARDS/acute lung injury. The influence of VEGF was investigated in a model of stretch-induced apoptosis. High-amplitude mechanical stretch induced the secretion of VEGF. High VEGF concentrations may prevent stretch-induced apoptosis by restoring stretch-impaired phospatidylinositol-3 kinase signalling.
    Background and objective: Vascular endothelial growth factor (VEGF) is strongly expressed in the alveolar epithelium. VEGF has been shown to exhibit protective as well as injurious effects in ARDS/acute lung injury. We therefore investigated the influence of VEGF in a model of stretch-induced apoptosis.
    Methods: Isolated rat alveolar type II (ATII) cells were subjected to high-amplitude cyclic mechanical stretch (40 per minute, 30% change in surface area) for 24 h. VEGF gene expression was investigated by real-time reverse transcription-PCR. Concentrations of VEGF in culture supernatants of stretched cells were determined by ELISA. Apoptosis of cells following stretching was assessed by flow cytometry.
    Results: Vascular endothelial growth factor gene expression increased during the first 4 h of stretching and then declined to a similar level to that of static control cells. VEGF concentrations in cell supernatants increased in response to mechanical stretch, as compared with those in supernatants of static control cells. Incubation of ATII cells with higher concentrations of VEGF (50 ng/mL) during stretching inhibited apoptosis, presumably by restoring stretch-impaired phosphatidylinositol-3 kinase signalling. However, blocking free VEGF in the supernatant with an anti-VEGF antibody did not influence stretch-induced apoptosis.
    Conclusions: These findings suggest that high-amplitude mechanical stretch induced secretion of VEGF, which in high concentrations, may prevent stretch-induced apoptosis. In this model, however, the protective influence of VEGF was not essential for survival of ATII cells subjected to high-amplitude mechanical stretch.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Male ; Models, Animal ; Phosphatidylinositol 3-Kinases ; Pulmonary Alveoli/cytology ; Pulmonary Alveoli/drug effects ; Pulmonary Alveoli/metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Stress, Mechanical ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor A/pharmacology
    Chemical Substances RNA, Messenger ; Vascular Endothelial Growth Factor A ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
    Language English
    Publishing date 2010-02
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 1435849-9
    ISSN 1440-1843 ; 1323-7799
    ISSN (online) 1440-1843
    ISSN 1323-7799
    DOI 10.1111/j.1440-1843.2009.01701.x
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4957: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article ; Online: Macrophage Migration Inhibitory Factor (MIF) Expression Increases during Myocardial Infarction and Supports Pro-Inflammatory Signaling in Cardiac Fibroblasts.

    Voss, Svenja / Krüger, Saskia / Scherschel, Katharina / Warnke, Svenja / Schwarzl, Michael / Schrage, Benedikt / Girdauskas, Evaldas / Meyer, Christian / Blankenberg, Stefan / Westermann, Dirk / Lindner, Diana

    Biomolecules

    2019  Volume 9, Issue 2

    Abstract: Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine known to play a major role in inflammatory diseases such as myocardial infarction (MI), where its expression increases. Cardio protective functions of MIF during ischemia have been ... ...

    Abstract Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine known to play a major role in inflammatory diseases such as myocardial infarction (MI), where its expression increases. Cardio protective functions of MIF during ischemia have been reported. Recently, the structurally related MIF-2 was identified and similar effects are assumed. We wanted to further investigate the role of MIF and MIF-2 on inflammatory processes during MI. Therefore, we subjected mice to experimentally induced MI by coronary occlusion for one and five days. During the acute phase of MI, the gene expression of Mif was upregulated in the infarct zone, whereas Mif-2 was downregulated, suggesting a minor role of MIF-2. Simulating ischemic conditions or mechanical stress in vitro, we demonstrated that Mif expression was induced in resident cardiac cells. To investigate possible auto /paracrine effects, cardiomyocytes and cardiac fibroblasts were individually treated with recombinant murine MIF, which in turn induced Mif expression and the expression of pro-inflammatory genes in cardiac fibroblasts. Cardiomyocytes did not respond to recombinant MIF with pro-inflammatory gene expression. While MIF stimulation alone did not change the expression of pro-fibrotic genes in cardiac fibroblasts, ischemia reduced their expression. Mimicking the increased MIF levels during MI, we exposed cardiac fibroblasts to simulated ischemia in the presence of MIF, which led to further reduced expression of pro-fibrotic genes. The presented data show that MIF was expressed by resident cardiac cells during MI. In vitro, Mif expression was induced by different external stimuli in cardiomyocytes and cardiac fibroblasts. Addition of recombinant MIF protein increased the expression of pro-inflammatory genes in cardiac fibroblasts including Mif expression itself. Thereby, cardiac fibroblasts may amplify Mif expression during ischemia promoting cardiomyocyte survival.
    MeSH term(s) Animals ; Cells, Cultured ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Macrophage Migration-Inhibitory Factors/genetics ; Macrophage Migration-Inhibitory Factors/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Signal Transduction/genetics
    Chemical Substances Macrophage Migration-Inhibitory Factors
    Language English
    Publishing date 2019-01-23
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom9020038
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  6. Article ; Online: Precursor proadrenomedullin influences cardiomyocyte survival and local inflammation related to myocardial infarction.

    Hinrichs, Svenja / Scherschel, Katharina / Krüger, Saskia / Neumann, Johannes Tobias / Schwarzl, Michael / Yan, Isabell / Warnke, Svenja / Ojeda, Francisco M / Zeller, Tanja / Karakas, Mahir / Keller, Till / Meyer, Christian / Blankenberg, Stefan / Westermann, Dirk / Lindner, Diana

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

    2018  Volume 115, Issue 37, Page(s) E8727–E8736

    Abstract: Increased adrenomedullin (ADM) levels are associated with various cardiac diseases such as myocardial infarction (MI). ADM is cleaved off from the full-length precursor protein proadrenomedullin (ProADM) during its posttranslational processing. To date, ... ...

    Abstract Increased adrenomedullin (ADM) levels are associated with various cardiac diseases such as myocardial infarction (MI). ADM is cleaved off from the full-length precursor protein proadrenomedullin (ProADM) during its posttranslational processing. To date, no biological effect of ProADM is reported, while ADM infusion leads to antiapoptotic effects and improved cardiac function. Using an MI mouse model, we found an induction of ProADM gene as well as protein expression during the early phase of MI. This was accompanied by apoptosis and increasing inflammation, which substantially influence the post-MI remodeling processes. Simulating ischemia in vitro, we demonstrate that ProADM expression was increased in cardiomyocytes and cardiac fibroblasts. Subsequently, we treated ischemic cardiomyocytes with either ProADM or ADM and found that both proteins increased survival. This effect was diminishable by blocking the ADM
    MeSH term(s) Adrenomedullin/genetics ; Adrenomedullin/metabolism ; Adrenomedullin/pharmacology ; Aged ; Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Cells, Cultured ; Cytokines/metabolism ; Female ; Gene Expression/genetics ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Male ; Mice, Inbred C57BL ; Middle Aged ; Myocardial Infarction/genetics ; Myocardial Infarction/metabolism ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Protein Precursors/genetics ; Protein Precursors/metabolism ; Protein Precursors/pharmacology
    Chemical Substances Cytokines ; Inflammation Mediators ; Protein Precursors ; proadrenomedullin ; Adrenomedullin (148498-78-6)
    Language English
    Publishing date 2018-08-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1721635115
    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:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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