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}

@article{darkow_small_2021,
abstract = {In search of more efficacious and safe pharmacological treatments for atrial fibrillation (AF), atria-selective antiarrhythmic agents have been promoted that target ion channels principally expressed in the atria. This concept allows one to engage antiarrhythmic effects in atria, but spares the ventricles from potentially proarrhythmic side effects. It has been suggested that cardiac small conductance Ca2+-activated K+ (SK) channels may represent an atria-selective target in mammals including humans. However, there are conflicting data concerning the expression of SK channels in different stages of AF, and recent findings suggest that SK channels are upregulated in ventricular myocardium when patients develop heart failure. To address this issue, RNA-sequencing was performed to compare expression levels of three SK channels (KCNN1, KCNN2, and KCNN3) in human atrial and ventricular tissue samples from transplant donor hearts (no cardiac disease), and patients with cardiac disease in sinus rhythm or with AF. In addition, for control purposes expression levels of several genes known to be either chamber-selective or differentially expressed in AF and heart failure were determined. In atria, as compared to ventricle from transplant donor hearts, we confirmed higher expression of KCNN1 and KCNA5, and lower expression of KCNJ2, whereas KCNN2 and KCNN3 were statistically not differentially expressed. Overall expression of KCNN1 was low compared to KCNN2 and KCNN3. Comparing atrial tissue from patients with AF to sinus rhythm samples we saw downregulation of KCNN2 in AF, as previously reported. When comparing ventricular tissue from heart failure patients to non-diseased samples, we found significantly increased ventricular expression of KCNN3 in heart failure, as previously published. The other channels showed no significant difference in expression in either disease. Our results add weight to the view that SK channels are not likely to be an atria-selective target, especially in failing human hearts, and modulators of these channels may prove to have less utility in treating AF than hoped. Whether targeting SK1 holds potential remains to be elucidated.},
author = {Darkow, Elisa and Nguyen, Thong T. and Stolina, Marina and Kari, Fabian A. and Schmidt, Constanze and Wiedmann, Felix and Baczkó, István and Kohl, Peter and Rajamani, Sridharan and Ravens, Ursula and Peyronnet, Rémi},
doi = {10.3389/fphys.2021.650964},
issn = {1664-042X},
journal = {Frontiers in Physiology},
keywords = {+UsePublic, {\textgreater}UseGalaxy.eu},
month = {April},
note = {Publisher: Frontiers Media SA},
title = {Small {Conductance} {Ca2} \${\textbackslash}mathplus\$-{Activated} {K}\${\textbackslash}mathplus\$ ({SK}) {Channel} {mRNA} {Expression} in {Human} {Atrial} and {Ventricular} {Tissue}: {Comparison} {Between} {Donor}, {Atrial} {Fibrillation} and {Heart} {Failure} {Tissue}},
url = {https://doi.org/10.3389/fphys.2021.650964},
shorttitle = {Small {Conductance} {Ca2} +-{Activated} {K}+ ({SK}) {Channel} {mRNA} {Expression} in {Human} {Atrial} and {Ventricular} {Tissue}},
title = {Small {Conductance} {Ca2} +-{Activated} {K}+ ({SK}) {Channel} {mRNA} {Expression} in {Human} {Atrial} and {Ventricular} {Tissue}: {Comparison} {Between} {Donor}, {Atrial} {Fibrillation} and {Heart} {Failure} {Tissue}},
url = {https://www.frontiersin.org/article/10.3389/fphys.2021.650964},
urldate = {2022-03-18},
volume = {12},
year = {2021}
}
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year = {2020}
}

@article{guindo_tetragenococcus_2022,
abstract = {Tetragenococcus halophilus (T. halophilus) is a facultative anaerobic, coccus-shaped halophilic lactic acid-producing bacterium previously detected and cultured in various salty foods and credited for beneficial effects on human health. In this study, we investigated the presence of T. halophilus in human samples using a polyphasic approach including scanning electron microscopy, molecular biology methods and microbial culture. This unique investigation yielded the unprecedented presence of T. halophilus in human feces samples, thus enriching the repertoire of halophilic microorganisms colonizing the human gastrointestinal tract with the isolation and culture of T. halophilus for the first time in humans. Using the E-test strips, the MIC was assessed for T. halophilus strain CSURQ6002: rifampicin (MIC at 0.002 μg/mL), benzylpenicillin (MIC at 0.094 μg/mL), amoxicillin (MIC at 0.5 μg/mL), erythromycin (MIC at 2 μg/mL), clindamycin (MIC at 4 μg/mL), and vancomycin (MIC at 8 μg/mL). However, this strain showed a MIC up to 256 μg/mL for ciprofloxacin, fosfomycin, doxycyclin, imipenem, and colistin. In-silico profiling derived from whole genome sequencing (NCBI accession number: PRJNA780809), was confirmed. This discovery suggested that T. halophilus was part of the human digestive microbiota and that its potential role on human health should be considered.},
author = {Guindo, Cheick Oumar and Morsli, Madjid and Bellali, Sara and Drancourt, Michel and Grine, Ghiles},
doi = {10.1016/j.crmicr.2022.100112},
issn = {2666-5174},
journal = {Current Research in Microbial Sciences},
keywords = {+UsePublic, {\textgreater}UseGalaxy.eu, Human gut microbiota, Isolation and culture, Next-generation sequencing, Scanning electron microscopy},
language = {en},
month = {January},
pages = {100112},
title = {A {Tetragenococcus} halophilus human gut isolate},
url = {https://www.sciencedirect.com/science/article/pii/S2666517422000098},
urldate = {2022-02-21},
volume = {3},
year = {2022}
}

@article{haas_n-tp63_2019,
abstract = {Mucociliary epithelia provide a first line of defense against pathogens. Impaired regeneration and remodeling of mucociliary epithelia are associated with dysregulated Wnt/β-catenin signaling in chronic airway diseases, but underlying mechanisms remain elusive, and studies yield seemingly contradicting results. Employing the Xenopus mucociliary epidermis, the mouse airway, and human airway Basal cells, we characterize the evolutionarily conserved roles of Wnt/β-catenin signaling in vertebrates. In multiciliated cells, Wnt is required for cilia formation during differentiation. In Basal cells, Wnt prevents specification of epithelial cell types by activating ΔN-TP63, a master transcription factor, which is necessary and sufficient to mediate the Wnt-induced inhibition of specification and is required to retain Basal cells during development. Chronic Wnt activation leads to remodeling and Basal cell hyperplasia, which are reversible in vivo and in vitro, suggesting Wnt inhibition as a treatment option in chronic lung diseases. Our work provides important insights into mucociliary signaling, development, and disease.},
author = {Haas, Maximilian and Gómez Vázquez, José Luis and Sun, Dingyuan Iris and Tran, Hong Thi and Brislinger, Magdalena and Tasca, Alexia and Shomroni, Orr and Vleminckx, Kris and Walentek, Peter},
Expand Down Expand Up @@ -2949,6 +2968,23 @@ @article{morsli_direct_2021
year = {2021}
}

@article{mossad_gut_2022,
abstract = {Microglial function declines during aging. The interaction of microglia with the gut microbiota has been well characterized during development and adulthood but not in aging. Here, we compared microglial transcriptomes from young-adult and aged mice housed under germ-free and specific pathogen-free conditions and found that the microbiota influenced aging associated-changes in microglial gene expression. The absence of gut microbiota diminished oxidative stress and ameliorated mitochondrial dysfunction in microglia from the brains of aged mice. Unbiased metabolomic analyses of serum and brain tissue revealed the accumulation of N6-carboxymethyllysine (CML) in the microglia of the aging brain. CML mediated a burst of reactive oxygen species and impeded mitochondrial activity and ATP reservoirs in microglia. We validated the age-dependent rise in CML levels in the sera and brains of humans. Finally, a microbiota-dependent increase in intestinal permeability in aged mice mediated the elevated levels of CML. This study adds insight into how specific features of microglia from aged mice are regulated by the gut microbiota.},
author = {Mossad, Omar and Batut, Bérénice and Yilmaz, Bahtiyar and Dokalis, Nikolaos and Mezö, Charlotte and Nent, Elisa and Nabavi, Lara Susann and Mayer, Melanie and Maron, Feres José Mocayar and Buescher, Joerg M. and de Agüero, Mercedes Gomez and Szalay, Antal and Lämmermann, Tim and Macpherson, Andrew J. and Ganal-Vonarburg, Stephanie C. and Backofen, Rolf and Erny, Daniel and Prinz, Marco and Blank, Thomas},
copyright = {2022 The Author(s), under exclusive licence to Springer Nature America, Inc.},
doi = {10.1038/s41593-022-01027-3},
issn = {1546-1726},
journal = {Nature Neuroscience},
keywords = {{\textgreater}UseGalaxy.eu, Ageing, Microbiology, Microglia},
language = {en},
month = {March},
pages = {1--11},
title = {Gut microbiota drives age-related oxidative stress and mitochondrial damage in microglia via the metabolite {N6}-carboxymethyllysine},
url = {https://www.nature.com/articles/s41593-022-01027-3},
urldate = {2022-03-07},
year = {2022}
}

@article{muller-ruch_glp_2020,
abstract = {In biomedical research, enormous progress is being made and new candidates for putative medicinal products emerge. However, most published preclinical data are not conducted according to the standard Good Laboratory Practice (GLP). GLP is mandatory for preclinical analysis of Advanced Therapy Medicinal Products (ATMP) and thereby a prerequisite for planning and conduction of clinical trials. Not inconsiderable numbers of clinical trials are terminated earlier or fail – do inadequate testing strategies or missing specialized assays during the preclinical development contribute to this severe complex of problems? Unfortunately, there is also a lack of access to GLP testing results and OECD (Organisation for Economic Co-operation and Development) GLP guidelines are not yet adjusted to ATMP specialties. Ultimately, GLP offers possibilities to generate reliable and reproducible data. Therefore, this review elucidates different GLP aspects in drug development, speculates on reasons of putative low GLP acceptance in the scientific community and mentions solution proposals.},
author = {Müller-Ruch, Ulrike and Skorska, Anna and Lemcke, Heiko and Steinhoff, Gustav and David, Robert},
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