73 research outputs found

    Intraspecific Geographic Variation of Fragrances Acquired by Orchid Bees in Native and Introduced Populations

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    Male orchid bees collect volatiles, from both floral and non-floral sources, that they expose as pheromone analogues (perfumes) during courtship display. The chemical profile of these perfumes, which includes terpenes and aromatic compounds, is both species-specific and divergent among closely related lineages. Thus, fragrance composition is thought to play an important role in prezygotic reproductive isolation in euglossine bees. However, because orchid bees acquire fragrances entirely from exogenous sources, the chemical composition of male perfumes is prone to variation due to environmental heterogeneity across habitats. We used Gas Chromatography/Mass Spectrometry (GC/MS) to characterize the perfumes of 114 individuals of the green orchid bee (Euglossa aff. viridissima) sampled from five native populations in Mesoamerica and two naturalized populations in the southeastern United States. We recorded a total of 292 fragrance compounds from hind-leg extracts, and found that overall perfume composition was different for each population. We detected a pronounced chemical dissimilarity between native (Mesoamerica) and naturalized (U.S.) populations that was driven both by proportional differences of common compounds as well as the presence of a few chemicals unique to each population group. Despite these differences, our data also revealed remarkable qualitative consistency in the presence of several major fragrance compounds across distant populations from dissimilar habitats. In addition, we demonstrate that naturalized bees are attracted to and collect large quantities of triclopyr 2-butoxyethyl ester, the active ingredient of several commercially available herbicides. By comparing incidence values and consistency indices across populations, we identify putative functional compounds that may play an important role in courtship signaling in this species of orchid bee

    Overexpression of the aphid-induced serine protease inhibitor <i>CI2c </i>gene in barley affects the generalist green peach aphid, not the specialist bird cherry-oat aphid

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    <div><p>Aphids are serious pests in crop plants. In an effort to identify plant genes controlling resistance against aphids, we have here studied a protease inhibitor, CI2c in barley (<i>Hordeum vulgare</i> L.). The <i>CI2c</i> gene was earlier shown to be upregulated by herbivory of the bird cherry-oat aphid <i>(Rhopalosiphum padi</i> L.<i>)</i> in barley genotypes with moderate resistance against this aphid, but not in susceptible lines. We hypothesized that CI2c contributes to the resistance. To test this idea, cDNA encoding <i>CI2c</i> was overexpressed in barley and bioassays were carried out with <i>R</i>. <i>padi</i>. For comparison, tests were carried out with the green peach aphid (<i>Myzus persicae</i> Sulzer), for which barley is a poor host. The performance of <i>R</i>. <i>padi</i> was not different on the <i>CI2c</i>-overexpressing lines in comparison to controls in test monitoring behavior and fecundity. <i>M</i>. <i>persicae</i> preference was affected as shown in the choice test, this species moved away from control plants, but remained on the <i>CI2c</i>-overexpressing lines. <i>R</i>. <i>padi</i>-induced responses related to defense were repressed in the overexpressing lines as compared to in control plants or the moderately resistant genotypes. A putative susceptibility gene, coding for a β-1,3-glucanase was more strongly induced by aphids in one of the <i>CI2c</i>-overexpressing lines. The results indicate that the CI2c inhibitor in overexpressing lines affects aphid-induced responses by suppressing defense. This is of little consequence to the specialist <i>R</i>.<i>padi</i>, but causes lower non-host resistance towards the generalist <i>M</i>. <i>persicae</i> in barley.</p></div

    Measuring Health Utilities in Children and Adolescents: A Systematic Review of the Literature.

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    BACKGROUND: The objective of this review was to evaluate the use of all direct and indirect methods used to estimate health utilities in both children and adolescents. Utilities measured pre- and post-intervention are combined with the time over which health states are experienced to calculate quality-adjusted life years (QALYs). Cost-utility analyses (CUAs) estimate the cost-effectiveness of health technologies based on their costs and benefits using QALYs as a measure of benefit. The accurate measurement of QALYs is dependent on using appropriate methods to elicit health utilities. OBJECTIVE: We sought studies that measured health utilities directly from patients or their proxies. We did not exclude those studies that also included adults in the analysis, but excluded those studies focused only on adults. METHODS AND FINDINGS: We evaluated 90 studies from a total of 1,780 selected from the databases. 47 (52%) studies were CUAs incorporated into randomised clinical trials; 23 (26%) were health-state utility assessments; 8 (9%) validated methods and 12 (13%) compared existing or new methods. 22 unique direct or indirect calculation methods were used a total of 137 times. Direct calculation through standard gamble, time trade-off and visual analogue scale was used 32 times. The EuroQol EQ-5D was the most frequently-used single method, selected for 41 studies. 15 of the methods used were generic methods and the remaining 7 were disease-specific. 48 of the 90 studies (53%) used some form of proxy, with 26 (29%) using proxies exclusively to estimate health utilities. CONCLUSIONS: Several child- and adolescent-specific methods are still being developed and validated, leaving many studies using methods that have not been designed or validated for use in children or adolescents. Several studies failed to justify using proxy respondents rather than administering the methods directly to the patients. Only two studies examined missing responses to the methods administered with respect to the patients' ages

    HIV-2 interaction with cell coreceptors: amino acids within the V1/V2 region of viral envelope are determinant for CCR8, CCR5 and CXCR4 usage

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    © 2014 Santos-Costa et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Background: Human immunodeficiency virus 1 and 2 (HIV-1 and HIV-2) use cellular receptors in distinct ways. Besides a more promiscuous usage of coreceptors by HIV-2 and a more frequent detection of CD4-independent HIV-2 isolates, we have previously identified two HIV-2 isolates (HIV-2MIC97 and HIV-2MJC97) that do not use the two major HIV coreceptors: CCR5 and CXCR4. All these features suggest that in HIV-2 the Env glycoprotein subunits may have a different structural organization enabling distinct - although probably less efficient - interactions with cellular receptors. Results: By infectivity assays using GHOST cell line expressing CD4 and CCR8 and blocking experiments using CCR8-specific ligand, I-309, we show that efficient replication of HIV-2MIC97 and HIV-2MJC97 requires the presence of CCR8 at plasma cell membrane. Additionally, we disclosed the determinants of chemokine receptor usage at the molecular level, and deciphered the amino acids involved in the usage of CCR8 (R8 phenotype) and in the switch from CCR8 to CCR5 or to CCR5/CXCR4 usage (R5 or R5X4 phenotype). The data obtained from site-directed mutagenesis clearly indicates that the main genetic determinants of coreceptor tropism are located within the V1/V2 region of Env surface glycoprotein of these two viruses. Conclusions: We conclude that a viral population able to use CCR8 and unable to infect CCR5 or CXCR4-positive cells, may exist in some HIV-2 infected individuals during an undefined time period, in the course of the asymptomatic stage of infection. This suggests that in vivo alternate molecules might contribute to HIV infection of natural target cells, at least under certain circumstances. Furthermore we provide direct and unequivocal evidence that the usage of CCR8 and the switch from R8 to R5 or R5X4 phenotype is determined by amino acids located in the base and tip of V1 and V2 loops of HIV-2 Env surface glycoprotein.This work was supported by grants from: Fundação para a Ciência e Tecnologia (FCT; PPCDT/SAU-IMI/55726/2004); Fundação para a Ciência e Tecnologia and Ministério da Saúde de Portugal (VIH/SAU/0006/2011); and from Gilead Sciences Portugal (Programa Gilead Génese).info:eu-repo/semantics/publishedVersio

    Inflammation in Alzheimer’s Disease and Molecular Genetics: Recent Update

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    United We Stand: Population Based Methods for Solving Unknown POMDPs

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    The extracellular chaperone clusterin sequesters oligomeric forms of the amyloid-beta 1-40 peptide

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    In recent genome-wide association studies, the extracellular chaperone protein, clusterin, has been identified as a newly-discovered risk factor in Alzheimer\u27s disease. We have examined the interactions between human clusterin and the Alzheimer\u27s disease-associated amyloid-β 1-40 peptide (Aβ 1-40), which is prone to aggregate into an ensemble of oligomeric intermediates implicated in both the proliferation of amyloid fibrils and in neuronal toxicity. Using highly sensitive single-molecule fluorescence methods, we have found that Aβ 1-40 forms a heterogeneous distribution of small oligomers (from dimers to 50-mers), all of which interact with clusterin to form long-lived, stable complexes. Consequently, clusterin is able to influence both the aggregation and disaggregation of Aβ 1-40 by sequestration of the Aβ oligomers. These results not only elucidate the protective role of clusterin but also provide a molecular basis for the genetic link between clusterin and Alzheimer\u27s disease
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