Social Network Analysis and Mining to Monitor and Identify Problems with Large-Scale Information and Communication Technology Interventions

The published literature reveals several arguments concerning the strategic importance of information and communication technology (ICT) interventions for developing countries where the digital divide is a challenge. Large-scale ICT interventions can be an option for countries whose regions, both urban and rural, present a high number of digitally excluded people. Our goal was to monitor and identify problems in interventions aimed at certification for a large number of participants in different geographical regions. Our case study is the training at the Telecentros.BR, a program created in Brazil to install telecenters and certify individuals to use ICT resources. We propose an approach that applies social network analysis and mining techniques to data collected from Telecentros.BR dataset and from the socioeconomics and telecommunications infrastructure indicators of the participants’ municipalities. We found that (i) the analysis of interactions in different time periods reflects the objectives of each phase of training, highlighting the increased density in the phase in which participants develop and disseminate their projects; (ii) analysis according to the roles of participants (i.e., tutors or community members) reveals that the interactions were influenced by the center (or region) to which the participant belongs (that is, a community contained mainly members of the same region and always with the presence of tutors, contradicting expectations of the training project, which aimed for intense collaboration of the participants, regardless of the geographic region); (iii) the social network of participants influences the success of the training: that is, given evidence that the degree of the community member is in the highest range, the probability of this individual concluding the training is 0.689; (iv) the North region presented the lowest probability of participant certification, whereas the Northeast, which served municipalities with similar characteristics, presented high probability of certification, associated with the highest degree in social networking platform.     

Robust scaling in ecosystems and the meltdown of patch size distributions before extinction

Robust critical systems are characterized by power laws which occur over a broad range of conditions. Their robust behaviour has been explained by local interactions. While such systems could be widespread in nature, their properties are not well understood. Here, we study three robust critical ecosystem models and a null model that lacks spatial interactions. In all these models, individuals aggregate in patches whose size distributions follow power laws which melt down under increasing external stress. We propose that this power-law decay associated with the connectivity of the system can be used to evaluate the level of stress exerted on the ecosystem. We identify several indicators along the transition to extinction. These indicators give us a relative measure of the distance to extinction, and have therefore potential application to conservation biology, especially for ecosystems with self-organization and critical transitions.     

Unraveling the neuroprotective mechanisms of PrPC in excitotoxicity

Knowledge of the natural roles of cellular prion protein (PrP^C) is essential to an understanding of the molecular basis of prion pathologies. This GPI-anchored protein has been described in synaptic contacts, and loss of its synaptic function in complex systems may contribute to the synaptic loss and neuronal degeneration observed in prionopathy. In addition, Prnp knockout mice show enhanced susceptibility to several excitotoxic insults, GABA_A receptor-mediated fast inhibition was weakened, LTP was modified and cellular stress increased. Although little is known about how PrP^C exerts its function at the synapse or the downstream events leading to PrP^C-mediated neuroprotection against excitotoxic insults, PrP^C has recently been reported to interact with two glutamate receptor subunits (NR2D and GluR6/7). In both cases the presence of PrP^C blocks the neurotoxicity induced by NMDA and Kainate respectively. Furthermore, signals for seizure and neuronal cell death in response to Kainate in Prnp knockout mouse are associated with JNK3 activity, through enhancing the interaction of GluR6 with PSD-95. In combination with previous data, these results shed light on the molecular mechanisms behind the role of PrP^C in excitotoxicity. Future experimental approaches are suggested and discussed.     

Parasitism and maintenance of diversity in a fungal vegetative incompatibility system: the role of selection by deleterious cytoplasmic elements

In fungi, horizontal transmission of deleterious cytoplasmic elements is reduced by the vegetative incompatibility system. This self/non-self recognition system may select for greater diversity of fungal incompatibility phenotypes in a frequency-dependent manner but the link between the diversity of fungal phenotypes and the virulence of cytoplasmic parasites has been poorly studied. We used an epidemiological model to show that even when transmission between incompatibility types is permitted, parasite pressure can lead to high levels of polymorphism for vegetative incompatibility systems. Moreover, high levels of polymorphism in host populations can select for less virulent cytoplasmic parasites. This feedback mechanism between parasite virulence and vegetative incompatibility system polymorphism of host populations may account for the general avirulence of most known mycoviruses. Furthermore, this mechanism provides a new perspective on the particular ecology and evolution of the host/parasite interactions acting between fungi and their cytoplasmic parasites.     

Polyglutamine repeats and β‐helix structure: Molecular dynamics study

Neurodegenerative diseases are often associated with the formation of highly insoluble aggregates. Despite the efforts devoted to the characterization of these aggregates, their structure remains elusive. Several neurodegenerative diseases are characterized by the expansion of CAG repeats, which code for Gln. Among the structural models proposed for the aggregates observed in polyQ-linked diseases, the nanotube beta-helix model proposed by Perutz and colleagues Proc Natl Acad Sci U S A 2002;99:5591-5595 has been influential. In the present study, the stability of this beta-helix model has been investigated by performing molecular dynamics simulations on polyQ fragments of different lengths. The results indicate that models shorter than two full beta-helix turns are unstable and collapse toward irregular structures. On the other hand, longer beta-helix models, containing more than 40 residues, achieve a dynamic regular structure. This finding is in line with the observed threshold of Gln repeats (approximately 40) correlated with the insurgence of the disease. Notably, the structure of the final state of the models longer than 40 residues strictly depends on their size. A compact stable ellipsoidal structure is formed by the model made of two full helical turns (41 residues), whereas water filled tubular structures emerge from simulation on longer polypeptides. These results have been interpreted taking into account the experimental data on polyQ aggregates. A structural interpretation of the literature data has been proposed by assuming that different beta-helical models are involved in the different stages of the aggregation process.     

Hydrolysis of benzonitrile herbicides by soil actinobacteria and metabolite toxicity

The soil actinobacteria Rhodococcus rhodochrous PA-34, Rhodococcus sp. NDB 1165 and Nocardia globerula NHB-2 grown in the presence of isobutyronitrile exhibited nitrilase activities towards benzonitrile (approx. 1.1–1.9 U mg^?1 dry cell weight). The resting cell suspensions eliminated benzonitrile and the benzonitrile analogues chloroxynil (3,5-dichloro-4-hydroxybenzonitrile), bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) and ioxynil (3,5-diiodo-4-hydroxybenzonitrile) (0.5 mM each) from reaction mixtures at 30°C and pH 8.0. The products were isolated and identified as the corresponding substituted benzoic acids. The reaction rates decreased in the order benzonitrile ? chloroxynil > bromoxynil > ioxynil in all strains. Depending on the strain, 92–100, 70–90 and 30–51% of chloroxynil, bromoxynil and ioxynil, respectively, was hydrolyzed after 5 h. After a 20-h incubation, almost full conversion of chloroxynil and bromoxynil was observed in all strains, while only about 60% of the added ioxynil was converted into carboxylic acid. The product of ioxynil was not metabolized any further, and those of the other two herbicides very slowly. None of the nitrilase-producing strains hydrolyzed dichlobenil (2,6-dichlorobenzonitrile). 3,5-Dibromo-4-hydroxybenzoic acid exhibited less inhibitory effect than bromoxynil both on luminescent bacteria and germinating seeds of Lactuca sativa. 3,5-Diiodo-4-hydroxybenzoic acid only exhibited lower toxicity than ioxynil in the latter test.     

Interaction of copper(II) with the non-steroidal anti-inflammatory drugs naproxen and diclofenac: synthesis, structure, DNA- and albumin-binding

Copper(II) complexes with the non-steroidal anti-inflammatory drugs (NSAIDs) naproxen and diclofenac have been synthesized and characterized in the presence of nitrogen donor heterocyclic ligands (2,2′-bipyridine, 1,10-phenanthroline or pyridine). Naproxen and diclofenac act as deprotonated ligands coordinated to Cu(II) ion through carboxylato oxygens. The crystal structures of (2,2′-bipyridine)bis(naproxenato)copper(II), , (1,10-phenanthroline)bis(naproxenato)copper(II), and bis(pyridine)bis(diclofenac)copper(II), have been determined by X-ray crystallography. The UV study of the interaction of the complexes with calf-thymus DNA (CT DNA) has shown that the complexes can bind to CT DNA with (2,2′-bipyridine)bis(naproxenato)copper(II) exhibiting the highest binding constant to CT DNA. Competitive study with ethidium bromide (EB) indicates that the complexes can displace the DNA-bound EB suggesting strong competition with EB. The cyclic voltammograms of the complexes recorded in the presence of CT DNA have shown that the complexes can bind to CT DNA by the intercalative binding mode which has also been verified by DNA solution viscosity measurements. The NSAID ligands and their complexes exhibit good binding propensity to human or bovine serum albumin protein having relatively high binding constant values. The biological properties of the previously reported complexes [Cu₂(naproxenato)₄(H₂O)₂], [Cu₂(diclofenac)₄(H₂O)₂] and [Cu(naproxenato)₂(pyridine)₂(H₂O)] have been also evaluated. The dinuclear complexes exhibit similar affinity for CT DNA as the 2,2′-bipyridine or 1,10-phenanthroline containing complexes. The pyridine containing complexes exhibit the lowest affinity for CT DNA and the lowest ability to displace EB from its EB-DNA complex.