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The demonstration that interleukin 2 (IL-2) is a lectin specific for oligomannosides allows to understand a new function for this cytokine: as a bifunctional molecule when bound to its receptor ss, IL-2 associates the latter which the CD3/TCR complex, interacting with oligosaccharides of CD3 through its carbohydrate-recognition domain (Zanetta et al. , 1996, Biochem. J., 318, 49-53). This induces the tyrosine phosphorylation of the IL-2R beta by ++p56(lck) , the first step of the IL-2-dependent signaling. Since this specific association is disrupted in vitro by oligomannosides with five and six mannose residues, we made the hypothesis that pathogenic cells or microorganisms could bind IL-2, consequently disturbing the IL-2- dependent response. This study shows that the pathogenic yeast Candida albicans (in contrast with nonpathogenic yeasts) binds high amounts of IL-2 as did cancer cells. In contrast with cancer cells, yeasts do not bind the Man6GlcNAc2-specific lectin CSL, an endogenous "amplifier of activation signals" (Zanetta et al. , 1995, Biochem. J., 311, 629-636).   相似文献   
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A life cycle assessment (LCA) approach was used to examine the greenhouse gas (GHG) emissions and energy balance of short rotation coppice (SRC) willow for heat production. The modelled supply chain includes cutting multiplication, site establishment, maintenance, harvesting, storage, transport and combustion. The relative impacts of dry matter losses and methane emissions from chip storage were examined from a LCA perspective, comparing the GHG emissions from the SRC supply chain with those of natural gas for heat generation. The results show that SRC generally provides very high GHG emission savings of over 90 %. The LCA model estimates that a 1, 10 and 20 % loss of dry matter during storage causes a 1, 6 and 11 % increase in GHG emissions per MWh. The GHG emission results are extremely sensitive to emissions of methane from the wood chip stack: If 1 % of the carbon within the stack undergoes anaerobic decomposition to methane, then the GHG emissions per MWh are tripled. There are some uncertainties in the LCA results, regarding the true formation of methane in wood chip stacks, non-CO2 emissions from combustion, N2O emissions from leaf fall and the extent of carbon sequestered under the crop, and these all contribute a large proportion of the life cycle GHG emissions from cultivation of the crop.  相似文献   
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Background

Scabies is endemic in many Aboriginal and Torres Strait Islander communities, with 69% of infants infected in the first year of life. We report the outcomes against scabies of two oral ivermectin mass drug administrations (MDAs) delivered 12 months apart in a remote Australian Aboriginal community.

Methods

Utilizing a before and after study design, we measured scabies prevalence through population census with sequential MDAs at baseline and month 12. Surveys at months 6 and 18 determined disease acquisition and treatment failures. Scabies infestations were diagnosed clinically with additional laboratory investigations for crusted scabies. Non-pregnant participants weighing ≥15 kg were administered a single 200 μg/kg ivermectin dose, repeated after 2–3 weeks if scabies was diagnosed, others followed a standard alternative algorithm.

Principal Findings

We saw >1000 participants at each population census. Scabies prevalence fell from 4% at baseline to 1% at month 6. Prevalence rose to 9% at month 12 amongst the baseline cohort in association with an identified exposure to a presumptive crusted scabies case with a higher prevalence of 14% amongst new entries to the cohort. At month 18, scabies prevalence fell to 2%. Scabies acquisitions six months after each MDA were 1% and 2% whilst treatment failures were 6% and 5% respectively.

Conclusion

Scabies prevalence reduced in the six months after each MDA with a low risk of acquisition (1–2%). However, in a setting where living conditions are conducive to high scabies transmissibility, exposure to presumptive crusted scabies and population mobility, a sustained reduction in prevalence was not achieved.

Clinical Trial Registration

Australian New Zealand Clinical Trial Register (ACTRN—12609000654257).  相似文献   
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