Modelling and mapping how common guillemots balance their energy budgets over a full annual cycle

The ability of individual animals to balance their energy budgets throughout the annual cycle is important for their survival, reproduction and population dynamics. However, the annual cycles of many wild, mobile animals are difficult to observe and our understanding of how individuals balance their energy budgets throughout the year therefore remains poor. We developed a hierarchical Bayesian state-space model to investigate how key components of animal energy budgets (namely individual energy gain and storage) varied in space and time. Our model used biologger-derived estimates of time-activity budgets, locations and energy expenditure to infer year-round time series of energy income and reserves. The model accounted for seasonality in environmental drivers such as sea surface temperature and daylength, allowing us to identify times and locations of high energy gain. Our study system was a population of common guillemots Uria aalge breeding at a western North Sea colony. These seabirds manage their energy budgets by adjusting their behaviour and accumulating fat reserves. However, typically during severe weather conditions, birds can experience an energy deficit over a sustained period, leading to starvation and large-scale mortality events. We show that guillemot energy gain varied in both time and space. Estimates of guillemot body mass varied throughout the annual cycle and birds periodically experienced losses in mass. Mass losses were likely to have either been adaptive, or due to energetic bottlenecks, the latter leading to increased susceptibility to mortality. Guillemots tended to be lighter towards the edge of their spatial distribution. We describe a framework that combines biologging data, time-activity budget analysis and Bayesian state-space modelling to identify times and locations of high energetic reward or potential energetic bottlenecks in a wild animal population. Our approach can be extended to address ecological and conservation-driven questions that were previously unanswerable due to logistical complexities in collecting data on wild, mobile animals across full annual cycles

Incorporating density‐dependent regulation into impact assessments for seabirds

1. Many industries are required to perform population viability analysis (PVA) during the consenting process for new developments to establish potential impacts on protected populations. However, these assessments rarely account for density-dependent regulation of demographic rates. Excluding density-dependent regulation from PVA-based impact assessments is often assumed to provide a maximum estimate of impact and therefore offer a precautionary approach to assessment. However, there is also concern that this practice may unnecessarily impede the development of important industries, such as offshore renewable energy. 2. In this study, we assess density-dependent regulation of breeding success in 31 populations of seabird. We then quantify the strength and form of this regulation using eight different formulations. Finally, we use PVA to examine how each formulation influences the recreation of observed dynamics (i.e. model validation), as well as the predicted absolute and relative population response to an extrinsic threat (i.e. model projection). 3. We found evidence of both negative (n = 3) and positive (n = 5) regulation of seabird breeding success. In populations exhibiting negative regulation, excluding density-dependent regulation from PVA-based impact assessment allowed uncontrolled population growth, such that model outcomes became biologically implausible. By contrast, in populations exhibiting positive regulation, excluding density-dependent regulation provided an appropriate reconstruction of observed dynamics, but population decline was underestimated in some populations. We find that multiple formulations of density dependence perform comparably at the detection, validation and projection stages of analysis. However, we tentatively recommend using a log-linear or Weibull distribution to describe density-dependent regulation of seabird breeding success in impact assessments to balance accuracy with caution. Finally, we show that relative PVA metrics of impact assessment cannot necessarily be used to overcome PVA misspecification by assuming density independence in positively regulated populations. 4. Synthesis and applications: We suggest that a density-dependent approach when performing PVA-based assessments for seabird populations will prevent biologically unrealistic, unconstrained population growth and therefore ensure meaningful PVA metrics in populations experiencing negative regulation. It will also maintain a precautionary approach for populations experiencing positive regulation, crucial when estimating impacts for these more vulnerable populations. These conclusions have immediate international application within the consenting processes for marine industries

Sucrose Nonfermenting-Related Kinase Enzyme-Mediated Rho-Associated Kinase Signaling is Responsible for Cardiac Function.

BACKGROUND: Cardiac metabolism is critical for the functioning of the heart, and disturbance in this homeostasis is likely to influence cardiac disorders or cardiomyopathy. Our laboratory has previously shown that SNRK (sucrose nonfermenting related kinase) enzyme, which belongs to the AMPK (adenosine monophosphate-activated kinase) family, was essential for cardiac metabolism in mammals. Snrk global homozygous knockout (KO) mice die at postnatal day 0, and conditional deletion of Snrk in cardiomyocytes (Snrk cmcKO) leads to cardiac failure and death by 8 to 10 months. METHODS AND RESULTS: We performed additional cardiac functional studies using echocardiography and identified further cardiac functional deficits in Snrk cmcKO mice. Nuclear magnetic resonance-based metabolomics analysis identified key metabolic pathway deficits in SNRK knockdown cardiomyocytes in vitro. Specifically, metabolites involved in lipid metabolism and oxidative phosphorylation are altered, and perturbations in these pathways can result in cardiac function deficits and heart failure. A phosphopeptide-based proteomic screen identified ROCK (Rho-associated kinase) as a putative substrate for SNRK, and mass spec-based fragment analysis confirmed key amino acid residues on ROCK that are phosphorylated by SNRK. Western blot analysis on heart lysates from Snrk cmcKO adult mice and SNRK knockdown cardiomyocytes showed increased ROCK activity. In addition, in vivo inhibition of ROCK partially rescued the in vivo Snrk cmcKO cardiac function deficits. CONCLUSIONS: Collectively, our data suggest that SNRK in cardiomyocytes is responsible for maintaining cardiac metabolic homeostasis, which is mediated in part by ROCK, and alteration of this homeostasis influences cardiac function in the adult heart

An Environment-Sensitive Synthetic Microbial Ecosystem

Microbial ecosystems have been widely used in industrial production, but the inter-relationships of organisms within them haven't been completely clarified due to complex composition and structure of natural microbial ecosystems. So it is challenging for ecologists to get deep insights on how ecosystems function and interplay with surrounding environments. But the recent progresses in synthetic biology show that construction of artificial ecosystems where relationships of species are comparatively clear could help us further uncover the meadow of those tiny societies. By using two quorum-sensing signal transduction circuits, this research designed, simulated and constructed a synthetic ecosystem where various population dynamics formed by changing environmental factors. Coherent experimental data and mathematical simulation in our study show that different antibiotics levels and initial cell densities can result in correlated population dynamics such as extinction, obligatory mutualism, facultative mutualism and commensalism. This synthetic ecosystem provides valuable information for addressing questions in ecology and may act as a chassis for construction of more complex microbial ecosystems

Alpha-Toxin Induces Programmed Cell Death of Human T cells, B cells, and Monocytes during USA300 Infection

This investigation examines the influence of alpha-toxin (Hla) during USA300 infection of human leukocytes. Survival of an USA300 isogenic deletion mutant of hla (USA300Δhla) in human blood was comparable to the parental wild-type strain and polymorphonuclear leukocyte (PMN) plasma membrane permeability caused by USA300 did not require Hla. Flow cytometry analysis of peripheral blood mononuclear cells (PBMCs) following infection by USA300, USA300Δhla, and USA300Δhla transformed with a plasmid over-expressing Hla (USA300Δhla Comp) demonstrated this toxin plays a significant role inducing plasma membrane permeability of CD14+, CD3+, and CD19+ PBMCs. Rapid plasma membrane permeability independent of Hla was observed for PMNs, CD14+ and CD19+ PBMCs following intoxication with USA300 supernatant while the majority of CD3+ PBMC plasma membrane permeability induced by USA300 required Hla. Addition of recombinant Hla to USA300Δhla supernatant rescued CD3+ and CD19+ PBMC plasma membrane permeability generated by USA300 supernatant. An observed delay in plasma membrane permeability caused by Hla in conjunction with Annexin V binding and ApoBrdU Tunel assays examining PBMCs intoxicated with recombinant Hla or infected with USA300, USA300Δhla, USA300Δhla Comp, and USA300ΔsaeR/S suggest Hla induces programmed cell death of monocytes, B cells, and T cells that results in plasma membrane permeability. Together these findings underscore the importance of Hla during S. aureus infection of human tissue and specifically demonstrate Hla activity during USA300 infection triggers programmed cell death of human monocytes, T cells and B cells that leads to plasma membrane permeability

Epistatic Relationships between sarA and agr in Staphylococcus aureus Biofilm Formation

Background: The accessory gene regulator (agr) and staphylococcal accessory regulator (sarA) play opposing roles in Staphylococcus aureus biofilm formation. There is mounting evidence to suggest that these opposing roles are therapeutically relevant in that mutation of agr results in increased biofilm formation and decreased antibiotic susceptibility while mutation of sarA has the opposite effect. To the extent that induction of agr or inhibition of sarA could potentially be used to limit biofilm formation, this makes it important to understand the epistatic relationships between these two loci. Methodology/Principal Findings: We generated isogenic sarA and agr mutants in clinical isolates of S. aureus and assessed the relative impact on biofilm formation. Mutation of agr resulted in an increased capacity to forma biofilmin the 8325-4 laboratory strain RN6390 but had little impact in clinical isolates S. aureus. In contrast, mutation of sarA resulted in a reduced capacity to form a biofilm in all clinical isolates irrespective of the functional status of agr. This suggests that the regulatory role of sarA in biofilm formation is independent of the interaction between sarA and agr and that sarA is epistatic to agr in this context. This was confirmed by demonstrating that restoration of sarA function restored the ability to form a biofilm even in the corresponding agr mutants. Mutation of sarA in clinical isolates also resulted in increased production of extracellular proteases and extracellular nucleases, both of which contributed to the biofilm-deficient phenotype of sarA mutants. However, studies comparing different strains with and without proteases inhibitors and/or mutation of the nuclease genes demonstrated that the agr-independent, sarA-mediated repression of extracellular proteases plays a primary role in this regard. Conclusions and Significance: The results we report suggest that inhibitors of sarA-mediated regulation could be used to limit biofilm formation in S. aureus and that the efficacy of such inhibitors would not be limited by spontaneous mutation of agr in the human host

Measurement of forward charged hadron flow harmonics in peripheral PbPb collisions at √sNN = 5.02 TeV with the LHCb detector

Flow harmonic coefficients, v n , which are the key to studying the hydrodynamics of the quark-gluon plasma (QGP) created in heavy-ion collisions, have been measured in various collision systems and kinematic regions and using various particle species. The study of flow harmonics in a wide pseudorapidity range is particularly valuable to understand the temperature dependence of the shear viscosity to entropy density ratio of the QGP. This paper presents the first LHCb results of the second- and the third-order flow harmonic coefficients of charged hadrons as a function of transverse momentum in the forward region, corresponding to pseudorapidities between 2.0 and 4.9, using the data collected from PbPb collisions in 2018 at a center-of-mass energy of 5.02 TeV . The coefficients measured using the two-particle angular correlation analysis method are smaller than the central-pseudorapidity measurements at ALICE and ATLAS from the same collision system but share similar features

Study of CP violation in B0 → DK⋆(892)0 decays with D → Kπ(ππ), ππ(ππ), and KK final states

A measurement of CP-violating observables associated with the interference of B0 → D0K⋆ (892)0 and B0 → D¯ 0K⋆ (892)0 decay amplitudes is performed in the D0 → K∓π ±(π +π −), D0 → π +π −(π +π −), and D0 → K+K− fnal states using data collected by the LHCb experiment corresponding to an integrated luminosity of 9 fb−1 . CP-violating observables related to the interference of B0 s → D0K¯ ⋆ (892)0 and B0 s → D¯ 0K¯ ⋆ (892)0 are also measured, but no evidence for interference is found. The B0 observables are used to constrain the parameter space of the CKM angle γ and the hadronic parameters r DK⋆ B0 and δ DK⋆ B0 with inputs from other measurements. In a combined analysis, these measurements allow for four solutions in the parameter space, only one of which is consistent with the world average

The effect of simulated cataracts on drivers' hazard perception ability

Purpose. We investigated the extent to which simulated cataracts slow a driver's ability to anticipate potential traffic hazards, a skill that has been found to correlate with crash risk. in previous studies, we found a significant correlation between contrast sensitivity and hazard perception in a sample of older drivers. The present study allowed us to determine the causal direction of this relationship. This is important as it provides a better understanding of the mechanisms underlying the higher crash risk of drivers with cataracts. Methods. One hundred eighty-six drivers with normal vision completed a validated video-based hazard perception driving test, designed to measure hazard anticipation response times in dynamic scenes. They also completed a change detection task based on traffic hazards, which was designed to measure object detection times in static scenes. Participants undertook the tasks wearing either mild or moderate cataract simulation goggles, or wearing goggle frames without lenses. Results. Participants wearing moderate simulated cataract goggles were slower than the control group in both the hazard perception test, t(98.50) = -3.71, p < 0.001, and the hazard change detection task, t(124) = -13.86, p < 0.001. participants with the mild Simulated cataract goggles were slower than the control group in the hazard change detection task, t(114) = -4.04, p < 0.001, but not the hazard perception test, t(114) = -1.33, p = 0.19. Conclusions. Moderate levels of simulated cataract slowed drivers' ability to detect and anticipate traffic hazards enough to warrant road safety concerns, despite the fact that the vision of participants wearing the cataract goggles still complied with the minimum legal standard required for driving