Boje Simon (closecrack8)

53, 95% confidence interval (CI) 0.52-12.25, p = .25 and HR = 2.60, 95% CI 0.54-12.59, p = .24 respectively). TVF free survival was 92.8% vs. 93.5% in patients with versus without stent underexpansion >20% (HR = 1.01, 95% CI 0.21-4.88, p = .99) and 89.3% vs. 97.8% in patients with versus without any residual focal lesion including lumen compromising hematoma (HR = 4.64, 95% CI 0.55-39.22, p = .18). Conclusion Numerically higher TVF rates were observed in patients with a post PCI FFR ≤0.85 and clear focal residual disease as assessed with IVUS.Homeostasis is an essential concept to understand the stability of organisms and their adaptive behaviors when coping with external and internal assaults. Many hormones that take part in homeostatic control come in antagonistic pairs, such as glucagon and insulin reflecting the inflow and outflow compensatory mechanisms to control a certain internal variable, such as blood sugar levels. By including negative feedback loops homeostatic controllers can exhibit oscillations with characteristic frequencies. In this paper we demonstrate the associated frequency changes in homeostatic systems when individual controllers -in a set of interlocked feedback loops- gain control in response to environmental changes. Taking p53 as an example, we show how Per2, ATM and Mdm2 feedback loops -interlocked with p53- gain individual control in dependence to the level of DNA damage, and how each of these controllers provide certain functionalities in their regulation of p53. In unstressed cells, the circadian regulator Per2 ensures a basic p53 level to allow its rapid up-regulation in case of DNA damage. When DNA damage occurs the ATM controller increases the level of p53 and defends it towards uncontrolled degradation, which despite DNA damage, would drive p53 to lower values and p53 dysfunction. Mdm2 on its side keeps p53 at a high but sub-apoptotic level to avoid premature apoptosis. However, with on-going DNA damage the Mdm2 set-point is increased by HSP90 and other p53 stabilizers leading finally to apoptosis. An emergent aspect of p53 upregulation during cell stress is the coordinated inhibition of ubiquitin-independent and ubiquitin-dependent degradation reactions. Whether oscillations serve a function or are merely a by-product of the controllers are discussed in view of the finding that homeostatic control of p53, as indicated above, does in principle not require oscillatory homeostats.Shang et al. (2016. J. Cell Biol.https//doi.org/10.1083/jcb.201603081) reported that activation of lysosomal TRPA1 channels led to intracellular calcium transients and CGRP release from DRG neurons. We argue that both findings are more likely due to influx of insufficiently buffered extracellular calcium rather than lysosomal release.In contrast to lymph nodes, the lymphoid regions of the spleen-the white pulp-are located deep within the organ, yielding the trafficking paths of T cells in the white pulp largely invisible. In an intravital microscopy tour de force reported in this issue of Immunity, Chauveau et al. show that T cells perform unidirectional, perivascular migration through the enigmatic marginal zone bridging channels.Positron emission tomography (PET) has proven to be an invaluable tool in the staging and management of disease in oncology; however, [18F]fluorodeoxyglucose ([18F]FDG) remains the most widely used PET radiopharmaceutical despite large financial investment in novel radiotracer development. We report our perspective and experience of translating radiopharmaceuticals into clinical studies, discussing the PET development pipeline from a chemistry perspective. We hope that by identifying potential points of attrition along the pipeline and suggesting solutions to these problems, we may help others take their pre-clinical radiotracers into human studies. This review focuses primarily on the development of fluorine-18 radiopharmaceuticals, although the broader field of radiometal chemistry is