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Evaluation of a novel West Nile virus transmission control strategy that targets Culex tarsalis with endectocide-containing blood meals
No full textControl of arbovirus transmission remains focused on vector control through application of insecticides directly to the environment. However, these insecticide applications are often reactive interventions that can be poorly-targeted, inadequate for localized control during outbreaks, and opposed due to environmental and toxicity concerns. In this study, we developed endectocide-treated feed as a systemic endectocide for birds to target blood feeding Culex tarsalis, the primary West Nile virus (WNV) bridge vector in the western United States, and conducted preliminary tests on the effects of deploying this feed in the field. In lab tests, ivermectin (IVM) was the most effective endectocide tested against Cx. tarsalis and WNV-infection did not influence mosquito mortality from IVM. Chickens and wild Eurasian collared doves exhibited no signs of toxicity when fed solely on bird feed treated with concentrations up to 200 mg IVM/kg of diet, and significantly more Cx. tarsalis that blood fed on these birds died (greater than 80% mortality) compared to controls (less than 25% mortality). Mosquito mortality following blood feeding correlated with IVM serum concentrations at the time of blood feeding, which dropped rapidly after the withdrawal of treated feed. Preliminary field testing over one WNV season in Fort Collins, Colorado demonstrated that nearly all birds captured around treated bird feeders had detectable levels of IVM in their blood. However, entomological data showed that WNV transmission was non-significantly reduced around treated bird feeders. With further development, deployment of ivermectin-treated bird feed might be an effective, localized WNV transmission control tool
During low-grade intestinal inflammation, ingestion of Streptococcus Thermophilus CNRZ160 Limited the Lean Body Mass Loss in Older Adults
No full textA triple amino acid substitution at position 88/94/95 in glycoprotein gp2a of type 1 porcine reproductive and respiratory syndrome virus (prrsv1) is responsible for adaptation to marc-145 cells
No full textThe Meat Animal Research Center-145 (MARC-145) cell line has been proven to be valuable for viral attenuation regarding vaccine development and production. Cell-adaptation is necessary for the efficient replication of porcine reproductive and respiratory syndrome virus (PRRSV) in these cells. Multiple sequence analysis revealed consistent amino acid substitutions in GP2a (V88F, M94I, F95L) of MARC-145 cell-adapted strains. To investigate the putative effect of these substitutions, mutations at either position 88, 94, 95, and their combinations were introduced into two PRRSV1 (13V091 and IVI-1173) infectious clones followed by the recovery of viable recombinants. When comparing the replication kinetics in MARC-145 cells, a strongly positive effect on the growth characteristics of the 13V091 strain (+2.1 log10) and the IVI-1173 strain (+1.7 log10) compared to wild-type (WT) virus was only observed upon triple amino acid substitution at positions 88 (V88F), 94 (M94I), and 95 (F95L) of GP2a, suggesting that the triple mutation is a determining factor in PRRSV1 adaptation to MARC-145 cells
Prediction of pesticide emission potential to atmosphere from their molecular properties using the TyPol tool
No full textDo positional preferences cause welfare gains?
No full textWe examine conditions for which positional preferences for voluntary contribution to a public good can be welfare
enhancing in a one-shot public good game, where individuals may also enjoy a return from their contribution ranking. We show that positional preferences are welfare-increasing only under certain conditions. We find that when agents' positional preferences are homogeneous, they overinvest in the public good compared to equilibrium with no positional preferences, resulting in a zero-sum positional race with a higher public good provision. When agents have heterogeneous positional preferences, the overall impact on social welfare is positive when endowments are homogeneous
Eimeria tenella ROP kinase EtROP1 induces G0/G1 cell cycle arrest and inhibits host cell apoptosis
No full textCoccidia are obligate intracellular protozoan parasites responsible for human and veterinary diseases. Eimeria tenella, the etiologic agent of cecal coccidiosis, is a major pathogen of chickens. In Toxoplasma gondii, some kinases from the rhoptry compartment (ROP) are key virulence factors. ROP kinases hijack and modulate many cellular functions and pathways, allowing T. gondii survival and development. E. tenella's kinome comprises 28 putative members of the ROP kinase family; most of them are predicted, as pseudokinases and their functions have never been characterized. One of the predicted kinase, EtROP1, was identified in the rhoptry proteome of E. tenella sporozoites. Here, we demonstrated that EtROP1 is active, and the N-terminal extension is necessary for its catalytic kinase activity. Ectopic expression of EtROP1 followed by co-immunoprecipitation identified cellular p53 as EtROP1 partner. Further characterization confirmed the interaction and the phosphorylation of p53 by EtROP1. E. tenella infection or overexpression of EtROP1 resulted both in inhibition of host cell apoptosis and G0/G1 cell cycle arrest. This work functionally described the first ROP kinase from E. tenella and its non-canonical structure. Our study provides the first mechanistic insight into host cell apoptosis inhibition by E. tenella. EtROP1 appears as a new candidate for coccidiosis control
OrthoMaM v10: Scaling-Up Orthologous Coding Sequence and Exon Alignments with More than One Hundred Mammalian Genomes
No full textWe present version 10 of OrthoMaM, a database of orthologous mammalian markers. OrthoMaM is already 11 years old and since the outset it has kept on improving, providing alignments and phylogenetic trees of high-quality computed with state-of-the-art methods on up-to-date data. The main contribution of this version is the increase in the number of taxa: 116 mammalian genomes for 14,509 one-to-one orthologous genes. This has been made possible by the combination of genomic data deposited in Ensembl complemented by additional good-quality genomes only available in NCBI. Version 10 users will benefit from pipeline improvements and a completely redesigned web-interface
Low-dose aspirin protective effects are correlated with deregulation of HNF factor expression in the preeclamptic placentas from mice and humans
No full textAspirin (acetyl-salicylic acid) is one of the most ancient drugs of the human pharmacopeia. Nonetheless, its action atlow doses is not well understood at the molecular level. One of the applications of low-dose aspirin treatment is theprevention of preeclampsia (PE) in patients at risk. Foeto-placental overexpression of the STOX1A transcription factor inmice triggers PE symptoms. Transcriptomic analysis of the placentas, showed that aspirin massively down-regulatesgenes of the coagulation and complement cascade, as well as genes involved in lipid transport. The genes modifiedby aspirin treatment are not the ones that are modified by STOX1 overexpression, suggesting that aspirin could actdownstream, symptomatically on the preeclamptic disease. Bioinformatics analysis of the promoters of thederegulated genes showed that they are strongly enriched in HNF transcription factors-binding sites, in accordancewith existing literature showing their roles as regulators of coagulation. Two of these transcription factors,Hnf1βandHnf4αare found down-regulated by aspirin treatment. In parallel, we show that in human patient placentas, aspirin-induced deregulations of genes of the coagulation cascade are also observed. Finally, the expression of Hnf1βtargetsequences (Kif12,F2,Hnf4αpromoters and a synthetic concatemer of the Hnf1β-binding site) were investigated bytransfection in trophoblast cell models, with or without aspirin treatment and with or without STOX1A overexpression.In this model we observed that STOX1A and aspirin tended to synergize in the down-regulation of Hnf1βtarget genesin trophoblasts