Predicting the potential distribution of Vexillata (Nematoda: Ornithostrongylidae) and its hosts (Mammalia: Rodentia) within America.

Species distribution modelling has been a powerful tool to explore the potential distribution of parasites in wildlife, being the basis of studies on biogeography. Vexillata spp. are intestinal nematodes found in several species of mammalian hosts, such as rodents (Geomyoidea) and hares (Leporidae) in the Nearctic and northern Neotropical regions. In the present study, we modelled the potential distribution of Vexillata spp. and their hosts, using exclusively species from the Geomyidae and Heteromyidae families, in order to identify their distributional patterns. Bioclimatic and topographic variables were used to identify and predict suitable habitats for Vexillata and its hosts. Using these models, we identified that temperature seasonality is a significant environmental factor that influences the distribution of the parasite genus and its host. In particular, the geographical distribution is estimated to be larger than that predicted for its hosts. This suggests that the nematode has the potential to extend its geographical range and also its spectrum of host species. Increasing sample size and geographical coverage will contribute to recommendations for conservation of this host-parasite system.

Could the beta rebound in the EEG be suitable to realize a "brain switch"?

OBJECTIVE: Performing foot motor imagery is accompanied by a peri-imagery ERD and a post-imagery beta ERS (beta rebound). Our aim was to study whether the post-imagery beta rebound is a suitable feature for a simple "brain switch". Such a brain switch is a specifically designed brain-computer interface (BCI) with the aim to detect only one predefined brain state (e.g. EEG pattern) in ongoing brain activity. METHOD: One EEG (Laplacian) recorded at the vertex during cue-based brisk foot motor imagery was analysed in 5 healthy subjects. The peri-imagery ERD and the post-imagery beta rebound (ERS) were analysed in detail between 6 and 40Hz and classified with two support vector machines. RESULTS: The ERD was detected in ongoing EEG (simulation of asynchronous BCI) with a true positive rate (TPR) of 28.4%+/-13.5 and the beta rebound with a TPR of 59.2%+/-20.3. In single runs with 30 cues each, the TPR for beta rebound detection was 78.6%+/-12.8. The false positive rate was always kept below 10%. CONCLUSION: The findings suggest that the beta rebound at Cz during foot motor imagery is a relatively stable and reproducible phenomenon detectable in single EEG trials. SIGNIFICANCE: Our results indicate that the beta rebound is a suitable feature to realize a "brain switch" with one single EEG (Laplacian) channel only.

Bioerosion caused by the sea urchin Diadema Mexicanum (Echinodermata: Echinoidea) at Bahías de Huatulco, Western Mexico

Mexican Pacific sea urchin studies have been focused mainly on species distribution, ecology and fisheries. Reef degradation by sea urchin bioerosion has not been studied previously en these reefs. We investigate the importance of Diadema mexicanum as a bioerosive agent of coral carbonate at Bahias de Huatulco, and the relative magnitude of coral accretion and bioerosion. At each of five localities in Bahias de Huatulco, sea urchin density, feeding and mechanical (spine) erosion was determined for three size class intervals. In general, D. mexicanum do not exert any significant role on coral reef community structure (live coral, dead coral or algal coverage) at the Huatulco area, probably because they are generally small (2.9-4 cm test size) and few in number (1.0-6.8 ind.m-2). Mean bioerosion rates are consistent with those measured for other diadematoids, as well as other urchin species in various eastern Pacific localities. However, the degree of bioerosive impact depends on species, test size, and population density of urchins. Coral carbonate removal by D. mexicanum erosion varies from 0.17 to 3.28 kgCaCO3m(-2)yr(-1). This represents a carbonate loss of < 5% of the annual coral carbonate production at Jicaral Chachacual, San Agustín and Isla Cacaluta, but 16 and 27% at Isla Montosa and La Entrega. On balance, coral accretion exceeds sea urchin erosion at all sites examined at Huatulco. At Bahias de Huatulco coral reef communities are actively growing, though in the coming years, it might be necessary to investigate the local effects of the interaction among erosion, and environmental and human induced perturbations

Bioerosion caused by the sea urchin Diadema Mexicanum (Echinodermata: Echinoidea) at Bahías de Huatulco, Western Mexico.

Mexican Pacific sea urchin studies have been focused mainly on species distribution, ecology and fisheries. Reef degradation by sea urchin bioerosion has not been studied previously en these reefs. We investigate the importance of Diadema mexicanum as a bioerosive agent of coral carbonate at Bahias de Huatulco, and the relative magnitude of coral accretion and bioerosion. At each of five localities in Bahias de Huatulco, sea urchin density, feeding and mechanical (spine) erosion was determined for three size class intervals. In general, D. mexicanum do not exert any significant role on coral reef community structure (live coral, dead coral or algal coverage) at the Huatulco area, probably because they are generally small (2.9-4 cm test size) and few in number (1.0-6.8 ind.m-2). Mean bioerosion rates are consistent with those measured for other diadematoids, as well as other urchin species in various eastern Pacific localities. However, the degree of bioerosive impact depends on species, test size, and population density of urchins. Coral carbonate removal by D. mexicanum erosion varies from 0.17 to 3.28 kgCaCO3m(-2)yr(-1). This represents a carbonate loss of < 5% of the annual coral carbonate production at Jicaral Chachacual, San Agustín and Isla Cacaluta, but 16 and 27% at Isla Montosa and La Entrega. On balance, coral accretion exceeds sea urchin erosion at all sites examined at Huatulco. At Bahias de Huatulco coral reef communities are actively growing, though in the coming years, it might be necessary to investigate the local effects of the interaction among erosion, and environmental and human induced perturbations.

Characterization of aspercetin, a platelet aggregating component from the venom of the snake Bothrops asper which induces thrombocytopenia and potentiates metalloproteinase-induced hemorrhage.

Thrombocytopenia occurs in a number of patients bitten by Bothrops asper, a species responsible for the majority of snakebites in Central America and southern Mexico. In this work we describe the isolation of a new platelet-aggregating protein, named aspercetin, from the venom of B. asper, which induces thrombocytopenia in mice. Isolation was carried out by a combination of ion-exchange chromatography on DEAE-Sepharose and affinity chromatography on Affi-Gel Blue. Aspercetin is a disulfide-linked heterodimer, with a pI of 4.5 and a molecular mass of 29,759 Da, detemined by MALDI-ESI mass spectrometry. N-terminal sequence shows homology with a number of venom proteins which belong to the C-type lectin family. Aspercetin has functional similarities with botrocetin, from B. jararaca venom, since it induces platelet aggregation only in the presence of plasma or purified von Willebrand factor. Aspercetin-mediated platelet aggregation results from the interaction of von Willebrand factor with platelet receptor GPIb. Aspercetin lacks anticoagulant effect and does not agglutinate erythrocytes, in contrast with other representatives of the C-type lectin family isolated from snake venoms. Moreover, aspercetin is not lethal, nor does it induce myonecrosis, hemorrhage and edema. When injected intravenously or intramuscularly in mice it induces a rapid, dose-dependent drop in platelet counts and prolongs the bleeding time, suggesting that it may play a role in the thrombocytopenia that develops in a number of B. asper envenomations. Moreover, mice injected intravenously with aspercetin and then receiving an intradermal injection of B. asper hemorrhagic metalloproteinase BaP1 develop a larger hemorrhagic lesion than mice receiving only BaP1. This suggests that aspercetin, by reducing platelet numbers, may

The venom of Bothrops asper from Guatemala: toxic activities and neutralization by antivenoms.

Bothrops asper is responsible for approximately half of the snakebite envenomations in Central America. Despite its medical relevance, only the venom of Costa Rican populations of this species has been studied to some detail, and there is very little information on intraspecies variability in venom composition and toxicity. Venom of B. asper from Guatemala was analyzed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis and two-dimensional gel electrophoresis, and its basic pharmacological activities were investigated with standard laboratory assays. Venom has lethal, hemorrhagic, myotoxic, edema-forming, coagulant, defibrinating and phospholipase A(2) activities, showing a similar toxicological profile to the one previously described for B. asper from Costa Rica. In addition, polyvalent antivenoms produced in Mexico and Costa Rica, and currently used in Guatemala, were tested for their ability to neutralize venom's toxic activities. Both antivenoms were effective against all effects studied, although the Costa Rican product showed higher potency against most activities tested and higher antibody titer against venom components, as determined by enzyme immunoassay. It is suggested that different dosage regimes should be considered when using these antivenoms in B. asper envenomations in Guatemala.

Effectiveness of batimastat, a synthetic inhibitor of matrix metalloproteinases, in neutralizing local tissue damage induced by BaP1, a hemorrhagic metalloproteinase from the venom of the snake bothrops asper.

Batimastat (BB-94), a synthetic hydroxamate peptidomimetic matrix metalloproteinase inhibitor, was tested for its ability to inhibit proteolytic and toxic effects induced by BaP1, a 24-kDa hemorrhagic metalloproteinase isolated from the venom of Bothrops asper, the medically most important snake species in Central America and southern Mexico. Batimastat inhibited proteolytic activity on biotinylated casein, with anIC(50) of 80 nM. In addition, batimastat was effective in inhibiting hemorrhagic, dermonecrotic, and edema-forming activities of this metalloproteinase if incubated with the enzyme prior to the assays. When the inhibitor was administered i.m. at the site of the toxin injection without preincubation, rapidly after metalloproteinase administration, it totally abrogated the hemorrhagic and dermonecrotic effects of BaP1. Inhibition was less effective as the time lapse between toxin and batimastat injection increased, due to the extremely rapid development of BaP1-induced local tissue damage in this experimental model. On the other hand, batimastat was ineffective if administered by the i.p. route immediately after toxin injection. It is concluded that batimastat, and probably other synthetic metalloproteinase inhibitors, may become useful therapeutic tools aimed at the in situ inhibition of venom metalloproteinases, when injected at the site of the bite rapidly after envenomation.

Inhibition of local hemorrhage and dermonecrosis induced by Bothrops asper snake venom: effectiveness of early in situ administration of the peptidomimetic metalloproteinase inhibitor batimastat and the chelating agent CaNa2EDTA.

The effectiveness of the chelating agent CaNa2EDTA and the peptidomimetic matrix metalloproteinase inhibitor batimastat (BB-94) to inhibit local tissue damage induced by Bothrops asper snake venom was studied in mice. Both compounds totally inhibited proteolytic, hemorrhagic, and dermonecrotic effects, and partially reduced edema-forming activity, when incubated with venom prior to injection. Much lower concentrations of batimastat than of CaNa2EDTA were required to inhibit these effects. In addition, batimastat, but not CaNa2EDTA, partially reduced myotoxic activity of the venom. When the inhibitors were administered at various time intervals after envenomation at the same site of venom injection, both compounds were effective in neutralizing local hemorrhage and dermonecrosis if administered rapidly after venom. Inhibition was not as effective as the time lapse between venom and inhibitor injections increased. Owing to the relevance of metalloproteinases in the pathogenesis of local tissue damage induced by B. asper and other pit viper venoms, it is suggested that administration of peptidomimetic metalloproteinase inhibitors or CaNa2EDTA at the site of venom injection may represent a useful alternative to complement antivenoms in the neutralization of venom-induced local tissue damage.