General relation between variance-time curve and power spectral density for point processes exhibiting 1/f β-fluctuations,with special reference to heart rate variability

Counting statistics in the form of the variance-time curve provides an alternative to spectral analysis for point processes exhibiting 1/f ^β-fluctuations, such as the heart beat. However, this is true only for β<1. Here, the case of general β is considered. To that end, the mathematical relation between the variance-time curve and power spectral density in the presence of 1/f ^β-noise is worked out in detail. A modified version of the variance-time curve is presented, which allows us to deal also with the case β?1. Some applications to the analysis of heart rate variability are given.     

The G2447A mutation does not affect ionization of a ribosomal group taking part in peptide bond formation

Peptide bond formation on the ribosome is catalyzed by RNA. Kinetic studies using Escherichia coli ribosomes have shown that catalysis (>10(5)-fold overall acceleration) is due to a large part to substrate positioning. However, peptide bond formation is inhibited approximately 100-fold by protonation of a ribosomal group with pKa=7.5, indicating either a contribution of general acid-base catalysis or inhibition by a pH-dependent conformational change within the active site. The function of a general base has been attributed to A2451 of 23S rRNA, and a charge relay system involving G2447 has been postulated to bring about the extensive pKa shift of A2451 implied in the model. Using a rapid kinetic assay, we found that the G2447A mutation, which has essentially no effect on cell growth, lowers the rate of peptide bond formation about 10-fold and does not affect the ionization of the ribosomal group with pKa=7.5 taking part in the reaction. This result does not support the proposed charge relay mechanism involving G2447 and the role of A2451 as general base in the catalysis of peptide bond formation.     

Species-specific probes and real-time PCR as a tool for fast detection and differentiation of 15 bacteria relevant in intensive care medicine

Detection of bacterial DNA from laboratory-prepared specimens such as water, urine, and blood has the potential to improve diagnostic tools in microbiology. A novel real-time PCR-based assay was developed and its performance and robustness were evaluated for a panel of spiked suspensions of 15 clinically relevant bacteria. As low as ten colony forming units (CFU)/100 μl were detectable. No cross-reactivity was observed, except for Staphylococcus aureus and Staphylococcus epidermidis. Nevertheless, S. aureus and S. epidermidis were reliably differentiated by melting curve analysis. The protocol was also validated with three groups containing a mixture of five spiked bacteria each, with the result of reliable differentiation. This novel assay allows an exact identification of 15 microbes relevant in intensive care medicine, including mixed infections, in a one run experiment in less than 4 h.     

Aphyly: identifying the flotsam and jetsam of systematics

Many taxon names in any classification will be composed of taxa that have yet to be demonstrated as monophyletic, that is, characterized by synapomorphies. Such taxa might be called aphyletic, the flotsam and jetsam in systematics, simply meaning they require taxonomic revision. The term aphyly is, however, the same as, if not identical to, Hennig's “Restkörper” and Bernardi's merophyly. None of these terms gained common usage. We outline Hennig's use of “Restkörper” and Bernardi's use of merophyly and compare it to aphyly. In our view, application of aphyly would avoid the oft made assumption that when a monophyletic group is discovered from within an already known and named taxon, then the species left behind are rendered paraphyletic. By identifying the flotsam and jetsam in systematics, we can focus on taxa in need of attention and avoid making phylogenetic faux pas with respect to their phylogenetic status.     

The oncogenic serine/threonine kinase Pim-1 directly phosphorylates and activates the G2/M specific phosphatase Cdc25C

The proto-oncogene Pim-1 encodes a serine-threonine kinase which is a downstream effector of cytokine signaling and can enhance cell cycle progression by altering the activity of several cell cycle regulators among them the G1 specific inhibitor p21(Waf), the phosphatase Cdc25A and the kinase C-TAK1. Here, we demonstrate by using biochemical assays that Pim-1 can interact with the phosphatase Cdc25C and is able to directly phosphorylate the N-terminal region of the protein. Cdc25C is functionally related to Cdc25A but acts specifically at the G2/M cell cycle transition point and can be inactivated by C-TAK1-mediated phosphorylation. Immuno-fluorescence experiments showed that Pim-1 and Cdc25C co-localize in the cytoplasm of both epithelial and myeloid cells. We find that phosphorylation by Pim-1 enhances the phosphatase activity of Cdc25C and in transfected cells that are arrested in G2/M by bleomycin, Pim-1 can enhance progression into G1. Therefore, we propose that Pim-1 activates Cdc25C by a direct phosphorylation and can thereby assume the function of a positive cell cycle regulator at the G2/M transition.     

Aboveground impacts of a belowground invader: how invasive earthworms alter aboveground arthropod communities in a northern North American forest

Declining arthropod communities have recently gained a lot of attention, with climate and land-use change among the most frequently discussed drivers. Here, we focus on a seemingly underrepresented driver of arthropod community decline: biological invasions. For approximately 12 000 years, earthworms have been absent from wide parts of northern North America, but they have been re-introduced with dramatic consequences. Most studies investigating earthworm-invasion impacts focus on the belowground world, resulting in limited knowledge on aboveground-community changes. We present observational data on earthworm, plant and aboveground arthropod communities in 60 plots, distributed across areas with increasing invasion status (low, medium and high) in a Canadian forest. We analysed how earthworm-invasion status and biomass impact aboveground arthropod community abundance, biomass and species richness, and how earthworm impacts cascade across trophic levels. We sampled approximately 13 000 arthropods, dominated by Hemiptera, Diptera, Araneae, Thysanoptera and Hymenoptera. Total arthropod abundance, biomass and species richness declined significantly from areas of low to those with high invasion status, with reductions of 61, 27 and 18%, respectively. Structural equation models suggest that earthworms directly and indirectly impact arthropods across trophic levels. We show that earthworm invasion can alter aboveground multi-trophic arthropod communities and suggest that belowground invasions might be underappreciated drivers of aboveground arthropod decline.     

The dsRNA-mimetic poly (I:C) and IL-18 synergize for IFNγ and TNFα expression

Interleukin (IL)-18 bioactivity and dsRNA sensing by receptors of innate immunity are key components of anti-viral host defense. Despite extensive data on signal transduction activated by both pathways knowledge on cross-communication is incomplete. By using human PBMC and predendritic KG1 cells, as prototypic IL-18-responsive cellular models, we sought to assess cytokine production under the influence of IL-18 and the dsRNA-mimetic poly (I:C). Here, we report on potent synergy between both mediators concerning pro-inflammatory IFNγ and TNFα production. KG1 data revealed that synergistic induction likely relied on TLR3 and was associated with prolonged/increased activation of NF-κB, as detected by IκB analysis and luciferase reporter assays, respectively. Moreover, extended activation of JNK was mediated by IL-18/poly (I:C). Although vital for innate immunity, overwhelming induction of inflammatory cytokines during viral infections poses the threat of serious collateral tissue damage. The stunning synergism inherent to IL-18/dsRNA-induced TNFα/IFNγ detected herein may contribute to this pathological phenomenon.