Eco‐evolutionary experience in novel species interactions

A better understanding of how ecological novelty influences interactions in new combinations of species is key for predicting interaction outcomes, and can help focus conservation and management efforts on preventing the introduction of novel organisms or species (including invasive species, GMOs, synthetic organisms, resurrected species and emerging pathogens) that seem particularly ‘risky’ for resident species. Here, we consider the implications of different degrees of eco‐evolutionary experience of interacting resident and non‐resident species, define four qualitative risk categories for estimating the probability of successful establishment and impact of novel species and discuss how the effects of novelty change over time. Focusing then on novel predator–prey interactions, we argue that novelty entails density‐dependent advantages for non‐resident species, with their largest effects often being at low prey densities. This is illustrated by a comparison of predator functional responses and prey predation risk curves between novel species and ecologically similar resident species, and raises important issues for the conservation of endangered resident prey species.     

Surface-templated fibril growth of peptide fragments from the shaft domain of the adenovirus fibre protein

Here we present a study of five analogues of a fragment from the shaft domain of the adenovirus fibre protein that readily form fibrils under a range of conditions. Using atomic force microscopy the fibrillisation of these peptides at the liquid/solid interface utilizing ordered crystalline substrates has been investigated. Our results demonstrate that the assembly pathway at the liquid/solid interface enables only the formation of truncated fibrillar structures, which align along the substrate's underlying atomic lattice during growth. Furthermore, that the concentration and volume of solution applied can be used to directly control the density of fibrillar coverage at the surface.     

Multi-disease data management system platform for vector-borne diseases

Background

Emerging information technologies present new opportunities to reduce the burden of malaria, dengue and other infectious diseases. For example, use of a data management system software package can help disease control programs to better manage and analyze their data, and thus enhances their ability to carry out continuous surveillance, monitor interventions and evaluate control program performance.

Methods and Findings

We describe a novel multi-disease data management system platform (hereinafter referred to as the system) with current capacity for dengue and malaria that supports data entry, storage and query. It also allows for production of maps and both standardized and customized reports. The system is comprised exclusively of software components that can be distributed without the user incurring licensing costs. It was designed to maximize the ability of the user to adapt the system to local conditions without involvement of software developers. Key points of system adaptability include 1) customizable functionality content by disease, 2) configurable roles and permissions, 3) customizable user interfaces and display labels and 4) configurable information trees including a geographical entity tree and a term tree. The system includes significant portions of functionality that is entirely or in large part re-used across diseases, which provides an economy of scope as new diseases downstream are added to the system at decreased cost.

Conclusions

We have developed a system with great potential for aiding disease control programs in their task to reduce the burden of dengue and malaria, including the implementation of integrated vector management programs. Next steps include evaluations of operational implementations of the current system with capacity for dengue and malaria, and the inclusion in the system platform of other important vector-borne diseases.     

Economic impact of cystic echinococcosis in peru

Background

Cystic echinococcosis (CE) constitutes an important public health problem in Peru. However, no studies have attempted to estimate the monetary and non-monetary impact of CE in Peruvian society.

Methods

We used official and published sources of epidemiological and economic information to estimate direct and indirect costs associated with livestock production losses and human disease in addition to surgical CE-associated disability adjusted life years (DALYs) lost.

Findings

The total estimated cost of human CE in Peru was U.S.$2,420,348 (95% CI:1,118,384–4,812,722) per year. Total estimated livestock-associated costs due to CE ranged from U.S.$196,681 (95% CI:141,641–251,629) if only direct losses (i.e., cattle and sheep liver destruction) were taken into consideration to U.S.$3,846,754 (95% CI:2,676,181–4,911,383) if additional production losses (liver condemnation, decreased carcass weight, wool losses, decreased milk production) were accounted for. An estimated 1,139 (95% CI: 861–1,489) DALYs were also lost due to surgical cases of CE.

Conclusions

This preliminary and conservative assessment of the socio-economic impact of CE on Peru, which is based largely on official sources of information, very likely underestimates the true extent of the problem. Nevertheless, these estimates illustrate the negative economic impact of CE in Peru.     

Arginase 2 deletion reduces neuro-glial injury and improves retinal function in a model of retinopathy of prematurity

Background

Retinopathy of prematurity (ROP) is a major cause of vision impairment in low birth weight infants. While previous work has focused on defining the mechanisms of vascular injury leading to retinal neovascularization, recent studies show that neurons are also affected. This study was undertaken to determine the role of the mitochondrial arginine/ornithine regulating enzyme arginase 2 (A2) in retinal neuro-glial cell injury in the mouse model of ROP.

Methods and Findings

Studies were performed using wild type (WT) and A2 knockout (A2−/−) mice exposed to Oxygen Induced Retinopathy (OIR). Neuronal injury and apoptosis were assessed using immunohistochemistry, TUNEL (terminal deoxynucleotidyl transferase dUTP nick end) labeling and Western blotting. Electroretinography (ERG) was used to assess retinal function. Neuro-glial injury in WT ROP mice was evident by TUNEL labeling, retinal thinning, decreases in number of rod bipolar cells and glial cell activation as compared with room air controls. Significant reduction in numbers of TUNEL positive cells, inhibition of retinal thinning, preservation of the rod bipolar cells and prevention of glial activation were observed in the A2−/− retinas. Retinal function was markedly impaired in the WT OIR mice as shown by decreases in amplitude of the b-wave of the ERG. This defect was significantly reduced in A2−/− mice. Levels of the pro-apoptotic proteins p53, cleaved caspase 9, cytochrome C and the mitochondrial protein Bim were markedly increased in WT OIR retinas compared to controls, whereas the pro-survival mitrochondrial protein BCL-xl was reduced. These alterations were largely blocked in the A2−/− OIR retina.

Conclusions

Our data implicate A2 in neurodegeneration during ROP. Deletion of A2 significantly improves neuronal survival and function, possibly through the regulation of mitochondrial membrane permeability mediated apoptosis during retinal ischemia. These molecular events are associated with decreased activation of glial cells, suggesting a rescue effect on macroglia as well.     

The Same but Different: Language Use and Attitudes in Four Communities of Burkina Faso.

The Same but Different: Language Use and Attitudes in Four Communities of Burkina Faso. Stuart Showalter. Dallas: SIL International, 2001. 261 pp.     

Dynamics of Violence: Processes of Escalation and De-Escalation in Violent Group Conflicts

Dynamics of Violence: Processes of Escalation and De- Escalation in Violent Group Conflicts. Sociologus, Special Publication 1. Georg Elvert. Stephen Feuchtwang. and Dieter Neubert. eds. Berlin: Duncker and Humblot, 1999 290 pp.     

AFM studies on the role of the protein RdgC in bacterial DNA recombination

Genetic studies of rdgC in different bacterial systems suggest that it may play a role in replication and recombination. However, the exact function of the corresponding protein, RdgC, is unknown. In this study, we have imaged complexes of RdgC with both linear and supercoiled circular plasmid DNA using atomic force microscopy. We confirm that RdgC does not target any specific sequences in double-stranded DNA, as has been suggested from biochemical data. However, we detect an increased affinity of the protein to DNA ends, and an ability to promote bending of DNA. Similar binding preferences have been reported for enzymes involved in recombination. Protein complexes with supercoiled plasmid DNA further enabled us to study the effect of RdgC on DNA superstructure. At high concentrations of protein we observed promotion of DNA condensation. Recombination is largely enhanced by close contacts of distant regions along the DNA strands, as can occur, for instance, through condensation. Our data thus support a possible function of RdgC as a midwife of recombination.     

Dissection of a novel nuclear localization signal in open reading frame 29 of varicella-zoster virus

Open reading frame 29 (ORF29) of varicella-zoster virus (VZV) encodes a 120-kDa single-stranded DNA binding protein (ORF29p) that is not packaged in the virion and is expressed during latency. During lytic infection, ORF29p is localized primarily to infected cell nuclei. In contrast, ORF29p is found exclusively in the cytoplasm in neurons of the dorsal root ganglia obtained at autopsy from seropositive latently infected patients. ORF29p accumulates in the nuclei of neurons in dorsal root ganglia obtained at autopsy from patients with active zoster. The localization of this protein is, therefore, tightly correlated with the proposed VZV lytic/latent switch. In this report, we have investigated the nuclear import mechanism of ORF29p. We identified a novel nuclear targeting domain bounded by amino acids 9 to 154 of ORF29p that functions independent of other VZV-encoded factors. In vitro import assays in digitonin-permeabilized HeLa cells reveal that ORF29p is transported into the nucleus by a Ran-, karyopherin alpha- and beta-dependent mechanism. These data are further supported by the demonstration that a glutathione S-transferase-karyopherin alpha fusion interacts with ORF29p, but not with a protein containing a point mutation in its nuclear localization signal (NLS). Therefore, the region of ORF29p responsible for its nuclear targeting is also involved in the association with karyopherin alpha. As a result of this interaction, this noncanonical NLS appears to hijack the classical cellular nuclear import machinery. Elucidation of the mechanisms governing ORF29p nuclear targeting could shed light on the VZV reactivation process.