898 research outputs found

    Stress-Mediated Allee Effects Can Cause the Sudden Collapse of Honey Bee Colonies.

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    The recent rapid decline in global honey bee populations could have significant implications for ecological systems, economics and food security. No single cause of honey bee collapse has yet to be identified, although pesticides, mites and other pathogens have all been shown to have a sublethal effect. We present a model of a functioning bee hive and introduce external stress to investigate the impact on the regulatory processes of recruitment to the forager class, social inhibition and the laying rate of the queen. The model predicts that constant density-dependent stress acting through an Allee effect on the hive can result in sudden catastrophic switches in dynamical behaviour and the eventual collapse of the hive. The model proposes that around a critical point the hive undergoes a saddle-node bifurcation, and that a small increase in model parameters can have irreversible consequences for the entire hive. We predict that increased stress levels can be counteracted by a higher laying rate of the queen, lower levels of forager recruitment or lower levels of natural mortality of foragers, and that increasing social inhibition can not maintain the colony under high levels of stress. We lay the theoretical foundation for sudden honey bee collapse in order to facilitate further experimental and theoretical consideration

    Puromycin aminonucleoside induces oxidant-dependent DNA damage in podocytes in vitro and in vivo

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    A decline in podocyte number correlates with progression to glomerulosclerosis. A mechanism underlying reduced podocyte number is the podocyte's relative inability to proliferate in response to injury. Injury by the podocyte toxin puromycin aminonucleoside (PA) is mediated via reactive oxygen species (ROS). The precise role of ROS in the pathogenesis of PA-induced glomerulosclerosis remains to be determined. We sought to examine whether PA-induced ROS caused podocyte DNA damage, possibly accounting for the podocyte's inability to proliferate in response to PA. In vitro, podocytes were exposed to PA, with or without the radical scavenger 1,3-dimethyl-2-thiourea (DMTU). In vivo, male Sprague–Dawley rats were divided into experimental groups (n=6/group/time point): PA, PA with DMTU, and control, killed at days 1.5, 3, or 7. DNA damage was measured by DNA precipitation, apurinic/apyrimidinic site, Comet, and 8-hydroxydeoxyguanosine assays. Cell cycle checkpoint protein upregulation (by immunostaining and Western blotting), histopathology, and biochemical parameters were examined. DNA damage was increased in cultured podocytes that received PA, but not PA with DMTU. PA exposure activated specific cell cycle checkpoint proteins, with attenuation by DMTU. DNA repair enzymes were activated, providing evidence for attempted DNA repair. The PA-treated animals developed worse proteinuria and histopathologic disease and exhibited more DNA damage than the DMTU pretreated group. No significant apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining. A mechanism underlying the lack of podocyte proliferation following PA-induced injury in vitro and in vivo may be ROS-mediated DNA damage, with upregulation of specific cell cycle checkpoints leading to cell cycle arrest

    A Bayesian analysis of regularised source inversions in gravitational lensing

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    Strong gravitational lens systems with extended sources are of special interest because they provide additional constraints on the models of the lens systems. To use a gravitational lens system for measuring the Hubble constant, one would need to determine the lens potential and the source intensity distribution simultaneously. A linear inversion method to reconstruct a pixellated source brightness distribution of a given lens potential model was introduced by Warren & Dye. In the inversion process, a regularisation on the source intensity is often needed to ensure a successful inversion with a faithful resulting source. In this paper, we use Bayesian analysis to determine the optimal regularisation constant (strength of regularisation) of a given form of regularisation and to objectively choose the optimal form of regularisation given a selection of regularisations. We consider and compare quantitatively three different forms of regularisation previously described in the literature for source inversions in gravitational lensing: zeroth-order, gradient and curvature. We use simulated data with the exact lens potential to demonstrate the method. We find that the preferred form of regularisation depends on the nature of the source distribution.Comment: 18 pages, 10 figures; Revisions based on referee's comments after initial submission to MNRA

    Influence of Fabrication Technique on the Fiber Pushout Behavior in a Sapphire-Reinforced Nial Matrix Composite

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    Directional solidification (DS) of \u27\u27powder-cloth\u27\u27 (PC) processed sapphire-NiAl composites was carried out to examine the influence of fabrication technique on the fiber-matrix interfacial shear strength, measured using a fiber-pushout technique. The DS process replaced the fine, equiaxed NiAl grain structure of the PC composites with an oriented grain structure comprised of large columnar NiAl grains aligned parallel to the fiber axis, with fibers either completely engulfed within the NiAl grains or anchored at one to three grain boundaries. The load-displacement behavior during the pushout test exhibited an initial \u27\u27pseudoelastic\u27\u27 response, followed by an \u27\u27inelastic\u27\u27 response, and finally a \u27\u27frictional\u27\u27 sliding response. The fiber-matrix interfacial shear strength and the fracture behavior during fiber pushout were investigated using an interrupted pushout test and fractography, as functions of specimen thickness (240 to 730 mu m) and fabrication technique. The composites fabricated using the PC and the DS techniques had different matrix and interface structures and appreciably different interfacial shear strengths. In the DS composites, where the fiber-matrix interfaces were identical for all the fibers, the interfacial debond shear stresses were larger for the fibers embedded completely within the NiAl grains and smaller for the fibers anchored at a few grain boundaries. The matrix grain boundaries coincident on sapphire fibers were observed to be the preferred sites for crack formation and propagation. While the frictional sliding stress appeared to be independent of the fabrication technique, the interfacial debond shear stresses were larger for the DS composites compared to the PC composites. The study highlights the potential of the DS technique to grow single-crystal NiAl matrix composites reinforced with sapphire fibers, with fiber-matrix interfacial shear strength appreciably greater than that attainable by the current solid-state fabrication techniques

    Human rhinovirus-induced inflammatory responses are inhibited by phosphatidylserine containing liposomes

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    Human rhinovirus (HRV) infections are major contributors to the healthcare burden associated with acute exacerbations of chronic airway disease, such as chronic obstructive pulmonary disease and asthma. Cellular responses to HRV are mediated through pattern recognition receptors that may in part signal from membrane microdomains. We previously found Toll-like receptor signaling is reduced, by targeting membrane microdomains with a specific liposomal phosphatidylserine species, 1-stearoyl-2-arachidonoyl-sn-glycero-3-phospho-L-serine (SAPS). Here we explored the ability of this approach to target a clinically important pathogen. We determined the biochemical and biophysical properties and stability of SAPS liposomes and studied their ability to modulate rhinovirus-induced inflammation, measured by cytokine production, and rhinovirus replication in both immortalized and normal primary bronchial epithelial cells. SAPS liposomes rapidly partitioned throughout the plasma membrane and internal cellular membranes of epithelial cells. Uptake of liposomes did not cause cell death, but was associated with markedly reduced inflammatory responses to rhinovirus, at the expense of only modest non-significant increases in viral replication, and without impairment of interferon receptor signaling. Thus using liposomes of phosphatidylserine to target membrane microdomains is a feasible mechanism for modulating rhinovirus-induced signaling, and potentially a prototypic new therapy for viral-mediated inflammation
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