Determination of phytoextraction potential of plant speciesfor toxic elements in soils of abandoned sulphide-mining areas

This study has determined contamination levels in soils and plants from the Sa˜o Domingos mining area, Portugal, by k0-INAA. Total concentrations of As, Sb, Cr, Hg, Cu, Zn and Fe in soils were very high, exceeding the maximum limits in Portuguese legislation. Concentrations of toxic elements like As, Sb and Zn were highest in roots of Erica andevalensis, Juncus acutus, Agrostis castellana and Nicotiana glauca. Additionally, As, Br, Cr, Fe, Sb and Zn in all organs of most plants were above toxicity levels. Those species that accumulated relatively high concentrations of toxic elements in roots (and tops) may be cultivated for phytostabilisation of similar areas

Aqueous extract of pomegranate peels (Punica granatum) encapsulated by spray drying.

Tannins, as punicalagin, represent the predominant class of bioactive substances from pomegranate, concentrating mostly in the peels and fruit mesocarp. The aim of this study was to select the wall materials (gum Arabic, Capsul™ and maltodextrin) for microencapsulating by spray drying an aqueous extract with 14% insoluble solids obtained from pomegranate peels. It was observed no statistical differences on punicalagin concentration in all powdered products. However the agents Capsul™ and maltodextrin were responsible for the better retention of punicalagin in the powdered product. So the stability of dried extracts makes it suitable for industrial or in agricultural applications.IDS 2014. August 24-27. Editors: Julien Andrieu, Roman Peczalski, Séverine Vessot. Series Editor: Arun S. Mujumdar

Modelling adult Aedes aegypti and Aedes albopictus survival at different temperatures in laboratory and field settings.

BACKGROUND: The survival of adult female Aedes mosquitoes is a critical component of their ability to transmit pathogens such as dengue viruses. One of the principal determinants of Aedes survival is temperature, which has been associated with seasonal changes in Aedes populations and limits their geographical distribution. The effects of temperature and other sources of mortality have been studied in the field, often via mark-release-recapture experiments, and under controlled conditions in the laboratory. Survival results differ and reconciling predictions between the two settings has been hindered by variable measurements from different experimental protocols, lack of precision in measuring survival of free-ranging mosquitoes, and uncertainty about the role of age-dependent mortality in the field. METHODS: Here we apply generalised additive models to data from 351 published adult Ae. aegypti and Ae. albopictus survival experiments in the laboratory to create survival models for each species across their range of viable temperatures. These models are then adjusted to estimate survival at different temperatures in the field using data from 59 Ae. aegypti and Ae. albopictus field survivorship experiments. The uncertainty at each stage of the modelling process is propagated through to provide confidence intervals around our predictions. RESULTS: Our results indicate that adult Ae. albopictus has higher survival than Ae. aegypti in the laboratory and field, however, Ae. aegypti can tolerate a wider range of temperatures. A full breakdown of survival by age and temperature is given for both species. The differences between laboratory and field models also give insight into the relative contributions to mortality from temperature, other environmental factors, and senescence and over what ranges these factors can be important. CONCLUSIONS: Our results support the importance of producing site-specific mosquito survival estimates. By including fluctuating temperature regimes, our models provide insight into seasonal patterns of Ae. aegypti and Ae. albopictus population dynamics that may be relevant to seasonal changes in dengue virus transmission. Our models can be integrated with Aedes and dengue modelling efforts to guide and evaluate vector control, better map the distribution of disease and produce early warning systems for dengue epidemics

Sialic Acid Glycobiology Unveils Trypanosoma cruzi Trypomastigote Membrane Physiology.

Trypanosoma cruzi, the flagellate protozoan agent of Chagas disease or American trypanosomiasis, is unable to synthesize sialic acids de novo. Mucins and trans-sialidase (TS) are substrate and enzyme, respectively, of the glycobiological system that scavenges sialic acid from the host in a crucial interplay for T. cruzi life cycle. The acquisition of the sialyl residue allows the parasite to avoid lysis by serum factors and to interact with the host cell. A major drawback to studying the sialylation kinetics and turnover of the trypomastigote glycoconjugates is the difficulty to identify and follow the recently acquired sialyl residues. To tackle this issue, we followed an unnatural sugar approach as bioorthogonal chemical reporters, where the use of azidosialyl residues allowed identifying the acquired sugar. Advanced microscopy techniques, together with biochemical methods, were used to study the trypomastigote membrane from its glycobiological perspective. Main sialyl acceptors were identified as mucins by biochemical procedures and protein markers. Together with determining their shedding and turnover rates, we also report that several membrane proteins, including TS and its substrates, both glycosylphosphatidylinositol-anchored proteins, are separately distributed on parasite surface and contained in different and highly stable membrane microdomains. Notably, labeling for α(1,3)Galactosyl residues only partially colocalize with sialylated mucins, indicating that two species of glycosylated mucins do exist, which are segregated at the parasite surface. Moreover, sialylated mucins were included in lipid-raft-domains, whereas TS molecules are not. The location of the surface-anchored TS resulted too far off as to be capable to sialylate mucins, a role played by the shed TS instead. Phosphatidylinositol-phospholipase-C activity is actually not present in trypomastigotes. Therefore, shedding of TS occurs via microvesicles instead of as a fully soluble form

Pathogenesis of reproductive failure induced by Trypanosoma vivax in experimentally infected pregnant ewes

The present study was aimed at investigating the effect of experimental infection by Trypanosoma vivax in different\ud stages of pregnancy, determining the pathogenesis of reproductive failure, and confirming transplacental\ud transmission. We used 12 pregnant ewes distributed into four experimental groups: G1, was formed by three ewes\ud infected with T. vivax in the first third of pregnancy (30 days); G2 comprised three infected ewes in the final third of\ud pregnancy (100 days); G3 and G4 were composed of three non-infected ewes with the same gestational period,\ud respectively. Each ewe of G1 and G2 was inoculated with 1.25 × 105 tripomastigotes. Clinical examination,\ud determination of parasitemia, serum biochemistry (albumin, total protein, glucose, cholesterol, and urea), packed\ud cell volume (PCV), serum progesterone, and pathological examination were performed. Placenta, amniotic fluid,\ud blood and tissues from the fetuses and stillbirths were submitted to PCR. Two ewes of G1 (Ewe 1 and 3) presented\ud severe infection and died in the 34th and 35th days post-infection (dpi), respectively; but both fetuses were\ud recovered during necropsy. In G2, Ewe 5 aborted two fetuses on the 130th day (30 dpi) of pregnancy; and Ewe 6\ud aborted one fetus in the 140th day (40 dpi) of gestation. Ewes 2 and 4 delivered two weak lambs that died five\ud days after birth. Factors possibly involved with the reproductive failure included high parasitemia, fever, low PCV,\ud body score, serum glucose, total protein, cholesterol, and progesterone. Hepatitis, pericarditis, and encephalitis were\ud observed in the aborted fetuses. The presence of T. vivax DNA in the placenta, amniotic fluid, blood, and tissues\ud from the fetuses confirms the transplacental transmission of the parasite. Histological lesion in the fetuses and\ud placenta also suggest the involvement of the parasite in the etiopathogenesis of reproductive failure in ewes

Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets