Distinguishing Social from Nonsocial Navigation in Moving Animal Groups

Many animals, such as migrating shoals of fish, navigate in groups. Knowing the mechanisms involved in animal navigation is important when it comes to explaining navigation accuracy, dispersal patterns, population and evolutionary dynamics, and consequently, the design of conservation strategies. When navigating toward a common target, animals could interact socially by sharing available information directly or indirectly, or each individual could navigate by itself and aggregations may not disperse because all animals are moving toward the same target. Here we present an analysis technique that uses individual movement trajectories to determine the extent to which individuals in navigating groups interact socially, given knowledge of their target. The basic idea of our approach is that the movement directions of individuals arise from a combination of responses to the environment and to other individuals. We estimate the relative importance of these responses, distinguishing between social and nonsocial interactions. We develop and test our method, using simulated groups, and we demonstrate its applicability to empirical data in a case study on groups of guppies moving toward shelter in a tank. Our approach is generic and can be extended to different scenarios of animal group movement. © 2012 by The University of Chicago

?2-Microglobulin Amyloid Fibril-Induced Membrane Disruption Is Enhanced by Endosomal Lipids and Acidic pH

Although the molecular mechanisms underlying the pathology of amyloidoses are not well understood, the interaction between amyloid proteins and cell membranes is thought to play a role in several amyloid diseases. Amyloid fibrils of ?2-microglobulin (?2m), associated with dialysis-related amyloidosis (DRA), have been shown to cause disruption of anionic lipid bilayers in vitro. However, the effect of lipid composition and the chemical environment in which ?2m-lipid interactions occur have not been investigated previously. Here we examine membrane damage resulting from the interaction of ?2m monomers and fibrils with lipid bilayers. Using dye release, tryptophan fluorescence quenching and fluorescence confocal microscopy assays we investigate the effect of anionic lipid composition and pH on the susceptibility of liposomes to fibril-induced membrane damage. We show that ?2m fibril-induced membrane disruption is modulated by anionic lipid composition and is enhanced by acidic pH. Most strikingly, the greatest degree of membrane disruption is observed for liposomes containing bis(monoacylglycero)phosphate (BMP) at acidic pH, conditions likely to reflect those encountered in the endocytic pathway. The results suggest that the interaction between ?2m fibrils and membranes of endosomal origin may play a role in the molecular mechanism of ?2m amyloid-associated osteoarticular tissue destruction in DRA

Vanadium

International audienceVanadium (chemical symbol, V) is a d-block transition metal,silver in color, appearing in the first long period of the peri-odic table between titanium and chromium. Vanadium hastwo stable isotopes: 50V and 51V, with atomic abundance of0.25 % and 99.75 %, respectively. Vanadium has several oxidation forms (between 2+ and 5+). In the lithosphere, Voccurs as reducing V(III) form, whereas in oxidizing con- ditions V prevails under V(IV) form. Vanadium(II) is partic- ularly unstable in the environment. Vanadium(III) is more stable than V(II), but it is also gradually oxidized by the air or dissolved oxygen. Vanadium(V) is expected to be the prevailing form in waters exposed to atmospheric oxygen, whereas V(IV) may be present in reducing environments. Depending upon geometry and environment, V ionic radii vary between 36 pm and 79 pm. Vanadium has a high melting point of 1910 42 C and is a mildly incompatible, refractory,lithophile (siderophile in the iron core and chondrites) ele- ment. Vanadium has an electronegativity of 1.63 on the Pau- ling scale and displays a first ionization potential of 6.74 eV. More details can be found in Richards (2006) and Haynes (2015)

Calculation of the visible-UV absorption spectra of hydrogen sulfide, bisulfide, polysulfides, and As and Sb sulfides, in aqueous solution

Recently we showed that visible-UV spectra in aqueous solution can be accurately calculated for arsenic (III) bisulfides, such as As(SH)(3), As(SH)(2)S(- )and their oligomers. The calculated lowest energy transitions for these species were diagnostic of their protonation and oligomerization state. We here extend these studies to As and Sb oxidation state III and v sulfides and to polysulfides S(n)(2-), n = 2–6, the bisulfide anion, SH(-), hydrogen sulfide, H(2)S and the sulfanes, S(n)H(2), n = 2–5. Many of these calculations are more difficult than those performed for the As(iii) bisulfides, since the As and Sb(v) species are more acidic and therefore exist as highly charged anions in neutral and basic solutions. In general, small and/or highly charged anions are more difficult to describe computationally than larger, monovalent anions or neutral molecules. We have used both Hartree-Fock based (CI Singles and Time-Dependent HF) and density functional based (TD B3LYP) techniques for the calculations of absorption energy and intensity and have used both explicit water molecules and a polarizable continuum to describe the effects of hydration. We correctly reproduce the general trends observed experimentally, with absorption energies increasing from polysulfides to As, Sb sulfides to SH(- )to H(2)S. As and Sb(v) species, both monomers and dimers, also absorb at characteristically higher energies than do the analogous As and Sb(III)species. There is also a small reduction in absorption energy from monomeric to dimeric species, for both As and Sb III and v. The polysufides, on the other hand, show no simple systematic changes in UV spectra with chain length, n, or with protonation state. Our results indicate that for the As and Sb sulfides, the oxidation state, degree of protonation and degree of oligomerization can all be determined from the visible-UV absorption spectrum. We have also calculated the aqueous phase energetics for the reaction of S(8 )with SH(- )to produce the polysulfides, S(n)H(-), n = 2–6. Our results are in excellent agreement with available experimental data, and support the existence of a S(6 )species

Tricholoma matsutake 1-Ocen-3-ol and methyl cinnamate repel mycophagous Proisotoma minuta (Collembola: Insecta)

Two major volatiles produced by the mycelia and fruiting bodies of Tricholoma matsutake (1-octen-3-ol and methyl cinnamate) repel a mycophagous collembolan, Proisotoma minuta. Aggregation of the collembolans on their diet was significantly inhibited by exposure to 1 ppm methyl cinnamate or 10 to 100 ppm 1-octen-3-ol. The aggregation activity decreased dose-dependently upon exposure to 1-octen-3-ol at concentrations higher than 0.01 ppm. Aggregation in the presence of methyl cinnamate exhibited three phases: no significant effect at concentrations ranging from 0.001 to 0.1 ppm, significant inhibition from 1 to 100 ppm, and strong inhibition at 1,000 ppm. These results may explain why certain collembolan species do not prefer T. matsutake fruiting bodies

Cellular Radiosensitivity: How much better do we understand it?

Purpose: Ionizing radiation exposure gives rise to a variety of lesions in DNA that result in genetic instability and potentially tumorigenesis or cell death. Radiation extends its effects on DNA by direct interaction or by radiolysis of H2O that generates free radicals or aqueous electrons capable of interacting with and causing indirect damage to DNA. While the various lesions arising in DNA after radiation exposure can contribute to the mutagenising effects of this agent, the potentially most damaging lesion is the DNA double strand break (DSB) that contributes to genome instability and/or cell death. Thus in many cases failure to recognise and/or repair this lesion determines the radiosensitivity status of the cell. DNA repair mechanisms including homologous recombination (HR) and non-homologous end-joining (NHEJ) have evolved to protect cells against DNA DSB. Mutations in proteins that constitute these repair pathways are characterised by radiosensitivity and genome instability. Defects in a number of these proteins also give rise to genetic disorders that feature not only genetic instability but also immunodeficiency, cancer predisposition, neurodegeneration and other pathologies. Conclusions: In the past fifty years our understanding of the cellular response to radiation damage has advanced enormously with insight being gained from a wide range of approaches extending from more basic early studies to the sophisticated approaches used today. In this review we discuss our current understanding of the impact of radiation on the cell and the organism gained from the array of past and present studies and attempt to provide an explanation for what it is that determines the response to radiation

Roadless wilderness area determines forest elephant movements in the Congo Basin

A dramatic expansion of road building is underway in the Congo Basin fuelled by private enterprise, international aid, and government aspirations. Among the great wilderness areas on earth, the Congo Basin is outstanding for its high biodiversity, particularly mobile megafauna including forest elephants (Loxodonta africana cyclotis). The abundance of many mammal species in the Basin increases with distance from roads due to hunting pressure, but the impacts of road proliferation on the movements of individuals are unknown. We investigated the ranging behaviour of forest elephants in relation to roads and roadless wilderness by fitting GPS telemetry collars onto a sample of 28 forest elephants living in six priority conservation areas. We show that the size of roadless wilderness is a strong determinant of home range size in this species. Though our study sites included the largest wilderness areas in central African forests, none of 4 home range metrics we calculated, including core area, tended toward an asymptote with increasing wilderness size, suggesting that uninhibited ranging in forest elephants no longer exists. Furthermore we show that roads outside protected areas which are not protected from hunting are a formidable barrier to movement while roads inside protected areas are not. Only 1 elephant from our sample crossed an unprotected road. During crossings her mean speed increased 14-fold compared to normal movements. Forest elephants are increasingly confined and constrained by roads across the Congo Basin which is reducing effective habitat availability and isolating populations, significantly threatening long term conservation efforts. If the current road development trajectory continues, forest wildernesses and the forest elephants they contain will collapse

Regulation of Neuronal APL-1 Expression by Cholesterol Starvation

Background: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the deposition of b-amyloid plaques composed primarily of the amyloid-b peptide, a cleavage product of amyloid precursor protein (APP). While mutations in APP lead to the development of Familial Alzheimer’s Disease (FAD), sporadic AD has only one clear genetic modifier: the e4 allele of the apolipoprotein E (ApoE) gene. Cholesterol starvation in Caenorhabditis elegans leads to molting and arrest phenotypes similar to loss-of-function mutants of the APP ortholog, apl-1 (amyloid precursor-like protein 1), and lrp-1 (lipoprotein receptor-related protein 1), suggesting a potential interaction between apl-1 and cholesterol metabolism. Methodology/Principal Findings: Previously, we found that RNAi knock-down of apl-1 leads to aldicarb hypersensitivity, indicating a defect in synaptic function. Here we find the same defect is recapitulated during lrp-1 knock-down and by cholesterol starvation. A cholesterol-free diet or loss of lrp-1 directly affects APL-1 levels as both lead to loss of APL-1::GFP fluorescence in neurons. However, loss of cholesterol does not affect global transcription or protein levels as seen by qPCR and Western blot. Conclusions: Our results show that cholesterol and lrp-1 are involved in the regulation of synaptic transmission, similar to apl-1. Both are able to modulate APL-1 protein levels in neurons, however cholesterol changes do not affect global apl-1 transcription or APL-1 protein indicating the changes are specific to neurons. Thus, regulation of synaptic transmission an

Prediction of specificity-determining residues for small-molecule kinase inhibitors

<p>Abstract</p> <p>Background</p> <p>Designing small-molecule kinase inhibitors with desirable selectivity profiles is a major challenge in drug discovery. A high-throughput screen for inhibitors of a given kinase will typically yield many compounds that inhibit more than one kinase. A series of chemical modifications are usually required before a compound exhibits an acceptable selectivity profile. Rationalizing the selectivity profile for a small-molecule inhibitor in terms of the specificity-determining kinase residues for that molecule can be an important step toward the goal of developing selective kinase inhibitors.</p> <p>Results</p> <p>Here we describe S-Filter, a method that combines sequence and structural information to predict specificity-determining residues for a small molecule and its kinase selectivity profile. Analysis was performed on seven selective kinase inhibitors where a structural basis for selectivity is known. S-Filter correctly predicts specificity determinants that were described by independent groups. S-Filter also predicts a number of novel specificity determinants that can often be justified by further structural comparison.</p> <p>Conclusion</p> <p>S-Filter is a valuable tool for analyzing kinase selectivity profiles. The method identifies potential specificity determinants that are not readily apparent, and provokes further investigation at the structural level.</p