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  1. Article ; Online: Biosafety Issues in Patient Transport during COVID-19: A Case Study on the Portuguese Emergency Services.

    Vandenberghe, Pierre / Ladeira, Luis Manuel / Gil, Margarida / Cardoso, Ivo / Rato, Fatima / Hayes, Jessica S / Connolly, Maire A / Gala, Jean-Luc

    International journal of environmental research and public health

    2024  Volume 21, Issue 1

    Abstract: During the COVID-19 pandemic, first responders faced significant biosafety challenges, especially while handling patient transport, potentially exposing them to infection. The PANDEM-2 (European project on pandemic preparedness and response) project, ... ...

    Abstract During the COVID-19 pandemic, first responders faced significant biosafety challenges, especially while handling patient transport, potentially exposing them to infection. The PANDEM-2 (European project on pandemic preparedness and response) project, funded by the Horizon 2020 program, sought to investigate the challenges confronting Emergency Medical Systems throughout the EU. First responders from Portugal's National Institute of Medical Emergency (INEM) were considered as a representative operational model of the national first responder agencies of European member states because they played a critical role during the COVID-19 pandemic. As a result, they were asked to complete an online survey about their COVID-19 pandemic-related professional activities. The survey focused on their perspectives on current biosafety guidelines and their operational practices. It covered opinions on existing protocols, technical concerns during patient transport, and issues after the patients arrived at the hospital. The key findings revealed concerns about risk assessment, the inadequacy of guidelines, and disparities in equipment access. This survey emphasizes the importance of developing streamlined, adaptable biosafety protocols, better coordination between prehospital and in-hospital services, and the development of scalable, cost-effective biosafety solutions. Based on our findings, we propose improvements to national and European biosafety directives and advocate for streamlined adaptation during pandemics.
    MeSH term(s) Humans ; Portugal/epidemiology ; Containment of Biohazards ; Pandemics ; COVID-19/epidemiology ; Emergency Medical Services
    Language English
    Publishing date 2024-01-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175195-X
    ISSN 1660-4601 ; 1661-7827
    ISSN (online) 1660-4601
    ISSN 1661-7827
    DOI 10.3390/ijerph21010099
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Potentiation of imatinib by cilostazol in sensitive and resistant gastrointestinal stromal tumor cell lines involves YAP inhibition.

    Vandenberghe, Pierre / Delvaux, Marine / Hagué, Perrine / Erneux, Christophe / Vanderwinden, Jean-Marie

    Oncotarget

    2019  Volume 10, Issue 19, Page(s) 1798–1811

    Abstract: Despite the introduction of tyrosine kinase inhibitors, gastrointestinal stromal tumors (GIST) resistance remains a major clinical challenge. We previously identified phosphodiesterase 3A (PDE3A) as a potential therapeutic target expressed in most GIST. ... ...

    Abstract Despite the introduction of tyrosine kinase inhibitors, gastrointestinal stromal tumors (GIST) resistance remains a major clinical challenge. We previously identified phosphodiesterase 3A (PDE3A) as a potential therapeutic target expressed in most GIST. The PDE3 inhibitor cilostazol reduced cell viability and synergized with the tyrosine kinase inhibitor imatinib (Gleevec™) in the imatinib-sensitive GIST882 cell line. Here, we found that cilostazol potentiated imatinib also in the imatinib-resistant GIST48 cell line. Cilostazol induced nuclear exclusion, hence inactivation, of the transcriptional co-activator YAP, in a cAMP-independent manner. Verteporfin, a YAP/TEAD interaction inhibitor, reduced by 90% the viability of both GIST882 and GIST48 cells. Our results highlight the potential use of compounds targeting PDE3A or YAP in combined multitherapy to tackle GIST resistance.
    Language English
    Publishing date 2019-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.26734
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Hyperplasia of interstitial cells of cajal in sprouty homolog 4 deficient mice.

    Thys, An / Vandenberghe, Pierre / Hague, Perrine / Klein, Ophir D / Erneux, Christophe / Vanderwinden, Jean-Marie

    PloS one

    2015  Volume 10, Issue 4, Page(s) e0124861

    Abstract: Gastrointestinal stromal tumors, which are thought to derive from interstitial cells of Cajal or their precursors, often harbor an oncogenic mutation of the KIT receptor tyrosine kinase. Sprouty homolog 4, a known negative regulator of ERK pathway, has ... ...

    Abstract Gastrointestinal stromal tumors, which are thought to derive from interstitial cells of Cajal or their precursors, often harbor an oncogenic mutation of the KIT receptor tyrosine kinase. Sprouty homolog 4, a known negative regulator of ERK pathway, has been identified in the interstitial cells of Cajal in the KitK641E murine model of gastrointestinal stromal tumors. Sprouty homolog 4 was upregulated both at the mRNA and protein level in these cells, suggesting that Sprouty homolog 4 is downstream of oncogenic KIT activation and potentially engaged in the negative feedback loop of ERK activation in this model. Here, we used KitK641E heterozygous and Sprouty homolog 4 knock out animals to quantify interstitial cells of Cajal in situ, using quantitative immunofluorescence for the receptor tyrosine kinase Kit and for phosphodiesterase 3a (PDE3A). In the antrum of Sprouty homolog 4 knock out mice, hyperplasia of interstitial cells of Cajal was reminiscent of the KitK641E heterozygous mice antrum. Additionally, the density of interstitial cells of Cajal was higher in the colon of adult Sprouty homolog 4 knock out mice than in WT littermates, although hyperplasia seemed more severe in KitK641E heterozygous mice. Functional transit studies also show similarities between Sprouty homolog 4 knock out and KitK641E heterozygous mice, as the total transit time in 9 month old animals was significantly increased in both genotypes compared to WT littermates. We concluded that the lack of Sprouty homolog 4 expression leads to hyperplasia of the interstitial cells of Cajal and is functionally associated with a delayed transit time.
    MeSH term(s) Animals ; Colon/metabolism ; Colon/pathology ; Cyclic Nucleotide Phosphodiesterases, Type 3/metabolism ; Disease Models, Animal ; Dwarfism/metabolism ; Dwarfism/pathology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Genotype ; Hyperplasia ; Interstitial Cells of Cajal/metabolism ; Interstitial Cells of Cajal/pathology ; Mice ; Mice, Knockout ; Microscopy, Fluorescence ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Pyloric Antrum/metabolism ; Pyloric Antrum/pathology ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Syndactyly/metabolism ; Syndactyly/pathology
    Chemical Substances Nerve Tissue Proteins ; Spry4 protein, mouse ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17) ; Pde3a protein, mouse (EC 3.1.4.17)
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0124861
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Phosphodiesterase 3A: a new player in development of interstitial cells of Cajal and a prospective target in gastrointestinal stromal tumors (GIST).

    Vandenberghe, Pierre / Hagué, Perrine / Hockman, Steven C / Manganiello, Vincent C / Demetter, Pieter / Erneux, Christophe / Vanderwinden, Jean-Marie

    Oncotarget

    2017  Volume 8, Issue 25, Page(s) 41026–41043

    Abstract: We previously identified phosphodiesterase 3A (PDE3A) as a marker for interstitial cells of Cajal (ICC) in adult mouse gut. However, PDE3A expression and function during gut development and in ICC-derived gastrointestinal stromal tumors (GIST) remained ... ...

    Abstract We previously identified phosphodiesterase 3A (PDE3A) as a marker for interstitial cells of Cajal (ICC) in adult mouse gut. However, PDE3A expression and function during gut development and in ICC-derived gastrointestinal stromal tumors (GIST) remained unknown. Here we found that PDE3A was expressed throughout ICC development and that ICC density was halved in PDE3A-deficient mice. In the human imatinib-sensitive GIST882 cell line, the PDE3 inhibitor cilostazol halved cell viability (IC50 0.35 μM) and this effect synergized with imatinib (Chou-Talalay's CI50 0.15). Recently the compound 6-(4-(diethylamino)-3-nitrophenyl)-5-methyl-4,5-dihydropyridazin-3(2H)-one, or DNMDP was found to be cytotoxic selectively for cells expressing both PDE3A and Schlafen12 (SLFN12) (de Waal L et al. Nat Chem Bio 2016), identifying a new, non-catalytic, role for PDE3A. 108 out of 117 (92%) of our human GIST samples displayed both PDE3A and SLFN12 immunoreactivity. GIST882 cells express both PDE3A and SLFN12 and DNMDP decreased their viability by 90%. Our results suggest a role for PDE3A during ICC development and open novel perspectives for PDE3A in targeted GIST therapy, on one hand by the synergism between imatinib and cilostazol, a PDE3 inhibitor already in clinical use for other indications, and, on the other hand, by the neomorphic, druggable, PDE3A-SLFN12 cytotoxic interplay.
    Language English
    Publishing date 2017-06-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.17010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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