933 resultados para British acting
Resumo:
An isolate of Gliocladium virens from disease affected soil in a commercial tomato greenhouse proved highly antagonistic to Fusarium oxysporum f.sp. lycopersici, used together with an isolate of the nematophagus fungus Verticillium chlamydosporium. Significant disease control was obtained when young mycelial preparation (on a food-base culture) of the G. virens together with V. chlamydosporium was applied in potting medium. Similar results were observed when a Trichoderma harzianum isolate was treated in combination with the V. chlamydosporium isolate. Most promising, in terms of minimizing the Fusarium wilt of tomato incidence, was also the effect of the bacteria associated with entomopathogenic nematodes (Steinernema spp.), Pseudomonas oryzihabitans and Xenorhabdus nematophilus.
Resumo:
1. Disease epizootics can significantly influence host population dynamics and the structure and functioning of ecological communities. Sarcoptic mange Sarcoptes scabiei has dramatically reduced red fox populations Vulpes vulpes in several countries, including Britain, although impacts on demographic processes are poorly understood. We review the literature on the impact of mange on red fox populations, assess its current distribution in Britain through a questionnaire survey and present new data on resultant demographic changes in foxes in Bristol, UK. 2. A mange epizootic in Sweden spread across the entire country in < 10 years resulting in a decline in fox density of up to 95%; density remained lowered for 15–20 years. In Spain, mange has been enzootic for > 75 years and is widely distributed; mange presence was negatively correlated with habitat quality. 3. Localized outbreaks have occurred sporadically in Britain during the last 100 years. The most recent large-scale outbreak arose in the 1990s, although mange has been present in south London and surrounding environs since the 1940s. The questionnaire survey indicated that mange was broadly distributed across Britain, but areas of perceived high prevalence (> 50% affected) were mainly in central and southern England. Habitat type did not significantly affect the presence/absence of mange or perceived prevalence rates. Subjective assessments suggested that populations take 15–20 years to recover. 4. Mange appeared in Bristol's foxes in 1994. During the epizootic phase (1994–95), mange spread through the city at a rate of 0.6–0.9 km/month, with a rise in infection in domestic dogs Canis familiaris c. 1–2 months later. Juvenile and adult fox mortality increased and the proportion of females that reproduced declined but litter size was unaffected. Population density declined by > 95%. 5. In the enzootic phase (1996–present), mange was the most significant mortality factor. Juvenile mortality was significantly higher than in the pre-mange period, and the number of juveniles classified as dispersers declined. Mange infection reduced the reproductive potential of males and females: females with advanced mange did not breed; severely infected males failed to undergo spermatogenesis. In 2004, Bristol fox population density was only 15% of that in 1994.
Resumo:
The interaction of the chemokine receptor, CCR5, expressed in recombinant cells, with different G proteins was investigated and CCR5 was found to interact with G(i), G(o) and G(q) species. Interaction with Gi leads to G protein activation, whereas G. does not seem to be activated. Additionally, CCR5 activation also leads to phosphorylation of Janus kinase 2 (JAK2). Activation of JAK2 is independent of Gi or Gq activation. Gi protein activation was not prevented by inhibition of JAK, showing that heterotrimeric G protein activation and activation of the JAK/signal transducer and activator of transcription (STAT) pathway are independent of each other. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Resumo:
The poliovirus cis-acting replication element (CRE) templates the uridylylation of VPg, the protein primer for genome replication. The CRE is a highly conserved structural RNA element in the enteroviruses and located within the polyprotein-coding region of the genome. We have determined the native structure of the CRE, defined the regions of the structure critical for activity, and investigated the influence of genomic location on function. Our results demonstrate that a 14-nucleotide unpaired terminal loop, presented on a suitably stable stem, is all that is required for function. These conclusions complement the recent analysis of the 14-nucleotide terminal loop in the CRE of human rhinovirus type 14. The CRE can be translocated to the 5' noncoding region of the genome, at least 3.7-kb distant from the native location, without adversely influencing activity, and CRE duplications do not adversely influence replication. We do not have evidence for a specific interaction between the CRE and the RNA-binding 3CD(pro) complex, an essential component of the uridylylation reaction, and the mechanism by which the CRE is coordinated and orientated during the reaction remains unclear. These studies provide a detailed overview of the structural determinants required for CRE function, and will facilitate a better understanding of the requirements for picornavirus replication.
Resumo:
Nucleotides in the terminal loop of the poliovirus 2C cis-acting replication element (2C(CRE)), a 61 nt structured RNA, function as the template for the addition of two uridylate (U) residues to the viral protein VPg. This uridylylation reaction leads to the formation of VPgpUpU, which is used by the viral RNA polymerase as a nucleotide-peptide primer for genome replication. Although VPg primes both positive- and negative-strand replication, the specific requirement for 2C(CRE)-mediated uridylylation for one or both events has not been demonstrated. We have used a cell-free in vitro translation and replication reaction to demonstrate that 2C(CRE) is not required for the initiation of the negative-sense strand, which is synthesized in the absence of 2C(CRE)-mediated VPgpUpU formation. We propose that the 3' poly(A) tail could serve as the template for the formation of a VPg-poly(U) primer that functions in the initiation of negative-sense strands.
Resumo:
Human selenium (Se) requirements are currently based on biochemical markers of Se status. In rats, tissue glutathione peroxidase-1 (Gpx1) mRNA levels can be used effectively to determine Se requirements; blood Gpx1 mRNA levels decrease in Se-deficient rats, so molecular biology-based markers have potential for human nutrition assessment. To study the efficacy of molecular biology markers for assessing Se status in humans, we conducted a longitudinal study on 39 subjects (age 45 +/- 11) in Reading, UK. Diet diaries (5 day) and blood were obtained from each subject at 2, 8, 17 and 23 weeks, and plasma Se, glutathione peroxidase (Gpx3) enzyme activity, and selenoprotein mRNA levels were determined. There were no significant longitudinal effects on Se biomarkers. Se intake averaged 48 +/- 14 mu g/d. Plasma Se concentrations averaged 1.13 +/- 0.16 mu mol/l. Plasma Se v. energy-corrected Se intake (ng Se/kJ/d) was significantly correlated, but neither Gpx3 activity v. Se intake (ng Se/kJ/d) nor Gpx3 activity v. plasma Se was significantly correlated. Collectively, this indicates that subjects were on the plateaus of the response curves. Selenoprotein mRNAs were quantitated in total RNA isolated from whole blood, but mRNA levels for Gpx1, selenoprotein H, and selenoprotein W (all highly regulated by Se in rodents), as well selenoprotein P, Gpx3, and phospholipid hydroperoxide glutathione peroxidase were also not significantly correlated with plasma Se. Thus selenoprotein molecular biomarkers, as well as traditional biochemical markers, are unable to further distinguish differences in Se status in these Se replete subjects. The efficacy of molecular biomarkers to detect Se deficiency needs to be tested in Se-deficient populations.
Resumo:
The article considers young people's occupational choices at the age of 15 in relation to their educational attainment, the occupations of their parents and their actual occupations when they are in their early 20s. It uses data from the British Household Panel Survey over periods of between five and ten years. The young people in the survey are occupationally ambitious: many more aspire to professional, managerial and technical jobs than the likely availability of these occupations. In general ambitions and educational attainment and intentions are well aligned but there are also many instances of misalignment; either people wanting jobs which their educational attainments and intentions will not prepare them for, or people with less ambitious aspirations than their educational performance would justify. Children from more occupationally advantaged families are more ambitious, achieve better educationally and have better occupational outcomes than other children. However, where young people are both ambitious and educationally successful the occupational outcomes are as good for those from disadvantaged as advantaged families. In contrast, where young people are neither ambitious nor educationally successful, the outcomes for those from disadvantaged homes are very much poorer than for other young people. The article suggests that while choice is real it is also heavily constrained for many people. A possible educational implication of the study is that career interventions could be directed at under-ambitious but academically capable young people from disadvantaged backgrounds.