Multiple predator species alter prey behavior, population growth, and a trophic cascade in a model estuarine food web

Predators can influence prey population dynamics by affecting prey behaviors with strong fitness consequences, with cascading effects on lower trophic levels. Here, we demonstrate that multiple predator species can nonconsumptively influence prey population growth and the strength of a trophic cascade in a model marine community. We exposed the herbivorous amphipod Ampithoe longimana to olfactory and visual cues from three common predators (pinfish, mud crabs, brown shrimp) singly and together in a multiple-predator assemblage to quantify the nonconsumptive effects (NCEs) of predator identity and the presence of multiple predators on prey population and community-level metrics. The presence of predator cues, particularly those of the pinfish and the multiple-predator treatments, decreased prey population growth and influenced primary and secondary production. To explore mechanisms underlying the observed NCEs in the experimental communities and their potential influence in the field, we quantified individual prey behavioral responses (changes in grazing rate, diet preference, dispersal, colonization) in the presence of predator cues. Predator cues decreased prey grazing, dispersal, and colonization but did not affect prey diet preference. Given the persistence of NCEs over time and the fact that trophic cascades are common features of marine systems, changes in marine predator communities may have widespread effects on predator-prey behavioral interactions with consequences for ecosystem function even in areas of weak predation pressure

General Relativistic Simulations of Magnetized Plasmas around Merging Supermassive Black Holes

Coalescing supermassive black hole binaries are produced by the mergers of galaxies and are the most powerful sources of gravitational waves accessible to space-based gravitational observatories. Some such mergers may occur in the presence of matter and magnetic fields and hence generate an electromagnetic counterpart. In this Letter, we present the first general relativistic simulations of magnetized plasma around merging supermassive black holes using the general relativistic magnetohydrodynamic code Whisky. By considering different magnetic field strengths, going from non-magnetically dominated to magnetically dominated regimes, we explore how magnetic fields affect the dynamics of the plasma and the possible emission of electromagnetic signals. In particular we observe a total amplification of the magnetic field of ~2 orders of magnitude which is driven by the accretion onto the binary and that leads to much stronger electromagnetic signals, more than a factor of 10^4 larger than comparable calculations done in the force-free regime where such amplifications are not possible.Comment: 7 pages, 5 figures. Minor changes to match version accepted for publication on The Astrophysical Journal Letter

Deciphering the Agonist Binding Mechanism to the Adenosine A1 Receptor.

Despite being among the most characterized G protein-coupled receptors (GPCRs), adenosine receptors (ARs) have always been a difficult target in drug design. To date, no agonist other than the natural effector and the diagnostic regadenoson has been approved for human use. Recently, the structure of the adenosine A1 receptor (A1R) was determined in the active, Gi protein complexed state; this has important repercussions for structure-based drug design. Here, we employed supervised molecular dynamics simulations and mutagenesis experiments to extend the structural knowledge of the binding of selective agonists to A1R. Our results identify new residues involved in the association and dissociation pathway, they suggest the binding mode of N6-cyclopentyladenosine (CPA) related ligands, and they highlight the dramatic effect that chemical modifications can have on the overall binding mechanism, paving the way for the rational development of a structure-kinetics relationship of A1R agonists.Leverhulme Trus

Travelling waves in pipe flow

A family of three-dimensional travelling waves for flow through a pipe of circular cross section is identified. The travelling waves are dominated by pairs of downstream vortices and streaks. They originate in saddle-node bifurcations at Reynolds numbers as low as 1250. All states are immediately unstable. Their dynamical significance is that they provide a skeleton for the formation of a chaotic saddle that can explain the intermittent transition to turbulence and the sensitive dependence on initial conditions in this shear flow.Comment: 4 pages, 5 figure

Probing the Interactions of Thiazole Abietane Inhibitors with the Human Serine Hydrolases ABHD16A and ABHD12

Peer reviewe

Is the Combination of Sulfonylureas and Metformin Associated With an Increased Risk of Cardiovascular Disease or All-Cause Mortality?: A meta-analysis of observational studies

OBJECTIVE—Observational studies assessing the association of combination therapy of metformin and sulfonylurea on all-cause and/or cardiovascular mortality in type 2 diabetes have shown conflicting results. We therefore evaluated the effects of combination therapy of sulfonylureas and metformin on the risk of all-cause mortality and cardiovascular disease (CVD) among people with type 2 diabetes

Evolution of turbulent spots in a parallel shear flow

The evolution of turbulent spots in a parallel shear flow is studied by means of full three-dimensional numerical simulations. The flow is bounded by free surfaces and driven by a volume force. Three regions in the spanwise spot cross-section can be identified: a turbulent interior, an interface layer with prominent streamwise streaks and vortices and a laminar exterior region with a large scale flow induced by the presence of the spot. The lift-up of streamwise streaks which is caused by non-normal amplification is clearly detected in the region adjacent to the spot interface. The spot can be characterized by an exponentially decaying front that moves with a speed different from that of the cross-stream outflow or the spanwise phase velocity of the streamwise roll pattern. Growth of the spots seems to be intimately connected to the large scale outside flow, for a turbulent ribbon extending across the box in downstream direction does not show the large scale flow and does not grow. Quantitatively, the large scale flow induces a linear instability in the neighborhood of the spot, but the associated front velocity is too small to explain the spot spreading.Comment: 10 pages, 10 Postscript figure

Nitric oxide from inflammatory origin impairs neural stem cell proliferation by inhibiting epidermal growth factor receptor signaling

Neuroinflammation is characterized by activation of microglial cells, followed by production of nitric oxide (NO), which may have different outcomes on neurogenesis, favoring or inhibiting this process. In the present study, we investigated how the inflammatory mediator NO can affect proliferation of neural stem cells (NSCs), and explored possible mechanisms underlying this effect. We investigated which mechanisms are involved in the regulation of NSC proliferation following treatment with an inflammatory stimulus (lipopolysaccharide plus IFN-gamma), using a culture system of subventricular zone (SVZ)-derived NSCs mixed with microglia cells obtained from wild-type mice (iNOS(+/+)) or from iNOS knockout mice (iNOS(-/-)). We found an impairment of NSC cell proliferation in iNOS(+/+) mixed cultures, which was not observed in iNOS(-/-) mixed cultures. Furthermore, the increased release of NO by activated iNOS(+/+) microglial cells decreased the activation of the ERK/MAPK signaling pathway, which was concomitant with an enhanced nitration of the EGF receptor. Preventing nitrogen reactive species formation with MnTBAP, a scavenger of peroxynitrite (ONOO-), or using the ONOO- degradation catalyst FeTMPyP cell proliferation and ERK signaling were restored to basal levels in iNOS(+/+) mixed cultures. Moreover, exposure to the NO donor NOC-18 (100 mu M), for 48 h, inhibited SVZ-derived NSC proliferation. Regarding the antiproliferative effect of NO, we found that NOC-18 caused the impairment of signaling through the ERK/MAPK pathway, which may be related to increased nitration of the EGF receptor in NSC. Using MnTBAP nitration was prevented, maintaining ERK signaling, rescuing NSC proliferation. We show that NO from inflammatory origin leads to a decreased function of the EGF receptor, which compromised proliferation of NSC. We also demonstrated that NO-mediated nitration of the EGF receptor caused a decrease in its phosphorylation, thus preventing regular proliferation signaling through the ERK/MAPK pathway.Foundation for Science and Technology, (FCT, Portugal); COMPETE; FEDER [PEst-C/SAU/LA0001/2013-2014, PEst-OE/EQB/LA0023/2013-2014, PTDC/SAU-NEU/102612/2008, PTDC/NEU-OSD/0473/2012]; FCT, Portugal [SERH/BPD/78901/2011, SERH/BD/38127/2007, SFRH/BD/77903/2011, SFRH/BD/79308/2011]info:eu-repo/semantics/publishedVersio