This review focuses on the available data regarding the utility of advanced left ventricular (LV) imaging in aortic stenosis (AS) and its potential impact for optimising the timing of aortic valve replacement. Ejection fraction is currently the only LV parameter recommended to guide intervention in AS. The cut-off value of 50%, recommended for decision-making in asymptomatic patients with AS, is currently under debate. Several imaging parameters have emerged as predictors of disease progression and clinical outcomes in this setting. Global longitudinal LV strain by speckle tracking echocardiography is useful for risk stratification of asymptomatic patients with severe AS and preserved LV ejection fraction. Its prognostic value was demonstrated in these patients, but further work is required to define the best thresholds to aid the decision-making process.  https://www.selleckchem.com/products/OSI-906.html  The assessment of myocardial fibrosis is the most studied application of cardiac magnetic resonance in AS. The detection of replacement fibrosis by late gadolinium enhancement offers incremental prognostic information in these patients. Clinical implementation of this technique to optimise the timing of aortic valve intervention in asymptomatic patients is currently tested in a randomised trial. The use of T1 mapping techniques can provide an assessment of interstitial myocardial fibrosis and represents an expanding field of interest. However, convincing data in patients with AS is still lacking. All these imaging parameters have substantial potential to influence the management decision in patients with AS in the future, but data from randomised clinical trials are awaited to define their utility in daily practice. © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.150 years after Louis Pasteur's germ theory ushered in the "golden age of microbiology" (1), infectious disease research is taking center stage again.…. Copyright © 2020 American Society for Microbiology.Apoptotic cell death can be an efficient defence reaction of mammalian cells infected with obligate intracellular pathogens the host cell dies and the pathogen cannot replicate. While this is well established for viruses, there is little experimental support for such a concept in bacterial infections. All Chlamydiales are obligate intracellular bacteria, and different species infect vastly different hosts. Chlamydia trachomatis (Ctr) infects human epithelial cells, Parachlamydia acanthamoebae (Pac) replicates in amoebae. We here report that apoptosis impedes growth of Pac in mammalian cells. In HeLa human epithelial cells, Pac-infection induced apoptosis, which was inhibited when mitochondrial apoptosis was blocked by co-deletion of the mediators of mitochondrial apoptosis, Bax and Bak, by over-expression of Bcl-XL or by deletion of the apoptosis-initiator Noxa. Deletion of Bax and Bak in mouse macrophages also inhibited apoptosis. Blocking apoptosis permitted growth of Pac in HeLa cells, as measured by fluorescence in situ hybridization, assessment of genome replication and protein synthesis and the generation of infectious progeny. Co-infection with Ctr inhibited Pac-induced apoptosis, suggesting that the known anti-apoptotic activity of Ctr can also block Pac-induced apoptosis. Ctr co-infection could not rescue Pac growth in HeLa in co-infected cells, Ctr even suppressed the growth of Pac independently of apoptosis, while Pac surprisingly enhanced the growth of Ctr Our results show that apoptosis can be used in the defence of mammalian cells against obligate intracellular bacteria and suggest that the known anti-apoptotic activity of human-pathogenic chlamydiae is indeed required to permit their growth in human cells. Copyright © 2020 American Society for Microbiology.Macrophages are a key cell type in innate immunity. Years of in vitro cell culture studies have unraveled myriad macrophage pathways that combat pathogens and how pathogen effectors subvert these mechanisms. However, in vitro cell culture studies may not accurately reflect how macrophages fit into the context of an innate immune response in whole animals with multiple cell types and tissues. Larval zebrafish have emerged as an intermediate model of innate immunity and host-pathogen interactions to bridge the gap between cell culture studies and mammalian models. These organisms possess an innate immune system largely conserved with humans and allow for state-of-the-art genetic and imaging techniques, all in the context of an intact organism. Using larval zebrafish, researchers are elucidating the function of macrophages in response to many different infections, including both bacterial and fungal pathogens. The goal of this review is to highlight studies in zebrafish that utilizing live imaging techniques to analyze macrophage activities in response to pathogens. Recent studies have explored the role of specific pathways and mechanisms in macrophage killing ability, explored how pathogens subvert these responses, identified subsets of macrophages with differential microbicidal activity, and implicated macrophages as an intracellular niche for pathogen survival and trafficking. Research in this model continues to advance our understanding of how macrophages, and specific pathways inside of these cells, fit into complex multicellular innate immune responses in vivo, providing important information on how pathogens evade these pathways and how we can exploit them for treatment development against microbial infections. Copyright © 2020 American Society for Microbiology.BEAF (Boundary Element-Associated Factor) was originally identified as a Drosophila melanogaster chromatin domain insulator binding protein, suggesting a role in gene regulation through chromatin organization and dynamics. Genome-wide mapping found that BEAF usually binds near transcription start sites, often of housekeeping genes, suggesting a role in promoter function. This would be a nontraditional role for an insulator binding protein. To gain insight into molecular mechanisms of BEAF function, we identified interacting proteins using yeast 2-hybrid assays. Here we focus on the transcription factor Sry-δ. Interactions were confirmed in pull-down experiments using bacterially expressed proteins, by bimolecular fluorescence complementation, and in a genetic assay in transgenic flies. Sry-δ interacted with promoter-proximal BEAF both when bound to DNA adjacent to BEAF or over 2 kb upstream to activate a reporter gene in transient transfection experiments. The interaction between BEAF and Sry-δ was detected using both a minimal developmental promoter (y) and a housekeeping promoter (RpS12), while BEAF alone strongly activated the housekeeping promoter.