Fully renewable limonene-derived polycarbonate as a high-performance alkyd resin

Limonene-derived polycarbonate-based alkyd resins (ARs) have been prepared by copolymerization of limonene dioxide with CO2, catalysed by a β-diiminate zinc–bis(trimethylsilyl)amido complex, and subsequent chemical modification with soybean oil fatty acids using triphenylethylphosphonium bromide as the catalyst. This quantitative partial modification was realized via epoxy–carboxylic acid chemistry, affording ARs with higher oil lengths, lower polydispersities and higher glass transition temperatures (Tg) in comparison to a conventional polyester AR based on phthalic acid, multifunctional polyol pentaerythritol and soybean fatty acid. The novel limonene polycarbonate AR and the conventional polyester AR were evaluated as coatings and both the physical drying (without the presence of the oxidative drying accelerator Borchi® Oxy Coat) and chemical curing (with Borchi® Oxy Coat) processes of these coatings were monitored by measuring the König hardness and complex modulus development with time. A better performance was obtained for the alkyd paint containing polycarbonates modified with fatty acids (FA-PCs), which showed a faster chemical drying, a higher König hardness and a higher Tg in coating evaluation, demonstrating that the fully renewable FA-PCs are promising resins for alkyd paint applications

Plant Stress-Tolerance Traits Predict Salt Marsh Vegetation Patterning

It is increasingly acknowledged that stressors can resonate across the boundaries between ecosystems. Salt marshes, vast areas shaped by ocean-shore interactions, constitute prime examples of ecosystems where multiple stress factors arising from one ecosystem act on the local community of another ecosystem. Although it is generally recognized that zonation of plant communities on salt marshes is strongly affected by marine stress factors associated with frequent flooding (salinity, anoxia), it is largely unknown what the isolated and interacting effect are of these different stressors. This calls for experiments to disentangle the relative effects of these single and interacting multiple stressors. In this study, we determined the single and interacting effects of two main abiotic stress factors on salt marshes: salinity and anoxia (as a result of flooding) and one biotic stress factor: soil compaction (as a result of livestock grazing) on the growth of the twelve dominant salt marsh plant species, using a full-factorial experiment. To link the experimental work to distributions of natural plant communities along a natural stress gradient, we related our experimental results to observed plant species distributions on a salt marsh that is exposed to all these three stressors. Salinity strongly affected ten species with two high-marsh species not surviving the highest salinity levels whereas anoxia only consistently affected growth of four species. Interestingly, we observed no synergistic effect of anoxia and salinity in salt marsh plants. Moreover, we observed a trade-off between the amount of aerenchyma and mechanical strength, indicating that species vary in their resistance to soil compaction. Overall, our results suggest that salinity is a major determinant of plant species composition on the salt marsh, followed by anoxia. The importance of soil compaction depends on salt marsh elevation: on the low marsh, increased oxygen supply by aerenchyma seems to outweigh resistance against mechanical stress whereas on the anaerobe low marsh, the reverse applies. Using the experimental data to predict cover of plant species in the field, our results suggest that the combination of plant responses to the various stressors may be a powerful predictor for explaining the plant composition on the salt marsh

Wild ducks excrete highly pathogenic avian influenza virus H5N8 (2014-2015) without clinical or pathological evidence of disease article

Highly pathogenic avian influenza (HPAI) is essentially a poultry disease. Wild birds have traditionally not been involved in its spread, but the epidemiology of HPAI has changed in recent years. After its emergence in southeastern Asia in 1996, H5 HPAI virus of the Goose/Guangdong lineage has evolved into several sub-lineages, some of which have spread over thousands of kilometers via long-distance migration of wild waterbirds. In order to determine whether the virus is adapting to wild waterbirds, we experimentally inoculated the HPAI H5N8 virus clade 2.3.4.4 group A from 2014 into four key waterbird species-Eurasian wigeon (Anas penelope), common teal (Anas crecca), mallard (Anas platyrhynchos), and common pochard (Aythya ferina)-and compared virus excretion and disease severity with historical data of the HPAI H5N1 virus infection from 2005 in the same four species. Our results showed that excretion was highest in Eurasian wigeons for the 2014 virus, whereas excretion was highest in common pochards and mallards for the 2005 virus. The 2014 virus infection was subclinical in all four waterbird species, while the 2005 virus caused clinical disease and pathological changes in over 50% of the common pochards. In chickens, the 2014 virus infection caused systemic disease and high mortality, similar to the 2005 virus. In conclusion, the evidence was strongest for Eurasian wigeons as long-distance vectors for HPAI H5N8 virus from 2014. The implications of the switch in species-specific virus excretion and decreased disease severity may be that the HPAI H5 virus more easily spreads in the wild-waterbird population

Prolonged Influenza Virus Shedding and Emergence of Antiviral Resistance in Immunocompromised Patients and Ferrets

Immunocompromised individuals tend to suffer from influenza longer with more serious complications than otherwise healthy patients. Little is known about the impact of prolonged infection and the efficacy of antiviral therapy in these patients. Among all 189 influenza A virus infected immunocompromised patients admitted to ErasmusMC, 71 were hospitalized, since the start of the 2009 H1N1 pandemic. We identified 11 (15%) cases with prolonged 2009 pandemic virus replication (longer than 14 days), despite antiviral therapy. In 5 out of these 11 (45%) cases oseltamivir resistant H275Y viruses emerged. Given the inherent difficulties in studying antiviral efficacy in immunocompromised patients, we have infected immunocompromised ferrets with either wild-type, or oseltamivir-resistant (H275Y) 2009 pandemic virus. All ferrets showed prolonged virus shedding. In wild-type virus infected animals treated with oseltamivir, H275Y resistant variants emerged within a week after infection. Unexpectedly, oseltamivir therapy still proved to be partially protective in animals infected with resistant virus. Immunocompromised ferrets offer an attractive alternative to study efficacy of novel antiviral therapies

Low pathogenic avian influenza A(H7N9) virus causes high mortality in ferrets upon intratracheal challenge: A model to study intervention strategies

Infections with low pathogenic avian influenza (LPAI) A(H7N9) viruses have caused more than 100 hospitalized human cases of severe influenza in China since February 2013 with a case fatality rate exceeding 25%. Most of these human infections presented with severe viral pneumonia, while limited information is available currently on the occurrence of mild and subclinical cases. In the present study, a ferret model for this virus infection in humans is presented to evaluate the pathogenesis of the infection in a mammalian host, as ferrets have been shown to mimic the pathogenesis of human infection with influenza viruses most closely. Ferrets were inoculated intratracheally with increasing doses (>10 e5 TCID50) of H7N9 influenza virus A/Anhui/1/2013 and were monitored for clinical and virological parameters up to four days post infection. Virus replication was detected in the upper and lower respiratory tracts while animals developed fatal viral pneumonia. This study illustrates the high pathogenicity of LPAI-H7N9 virus for mammals. Furthermore, the intratracheal inoculation route in ferrets proofs to offer a solid model for LPAI-H7N9 virus induced pneumonia in humans. This model will facilitate the development and assessment of clinical intervention strategies for LPAI-H7N9 virus infection in humans, such as preventive vaccination and the use of antivirals. (C) 2013 Elsevier Ltd. All rights reserved

Protein alignment of BsExlx1, PcExl1, EXPB1 and ScExlx1.

<p>Darker background indicates high amino acid conservation among the sequences. M1, M2 and M3 indicate the three classic motifs of plant expansins. The boxed amino acids are important residues involved in binding and creep activity in BsExlx1. White square indicates a putative N-glycosylation site in ScExlx1 and white circles indicate the predicted residues to form disulfide bonds.</p

Evolution of highly pathogenic H5N1 influenza A virus in the central nervous system of ferrets

Central nervous system (CNS) disease is the most common extra-respiratory tract complication of influenza A virus infections in humans. Remarkably, zoonotic highly pathogenic avian influenza (HPAI) H5N1 virus infections are more often associated with CNS disease than infections with seasonal influenza viruses. Evolution of avian influenza viruses has been extensively studied in the context of respiratory infections, but evolutionary processes in CNS infections remain poorly understood. We have previously observed that the ability of HPAI A/Indonesia/5/2005 (H5N1) virus to replicate in and spread throughout the CNS varies widely between individual ferrets. Based on these observations, we sought to understand the impact of entrance into and replication within the CNS on the evolutionary dynamics of virus populations. First, we identified and characterized three substitutions-PB1 E177G and A652T and NP I119M - detected in the CNS of a ferret infected with influenza A/Indonesia/5/2005 (H5N1) virus that developed a severe meningo-encephalitis. We found that some of these substitutions, individually or collectively, resulted in increased polymerase activity in vitro. Nevertheless, in vivo, the virus bearing the CNS-associated mutations retained its capacity to infect the CNS but showed reduced dispersion to other anatomical sites. Analyses of viral diversity in the nasal turbinate and olfactory bulb revealed the lack of a genetic bottleneck acting on virus populations accessing the CNS via this route. Furthermore, virus populations bearing the CNS-associated mutations showed signs of positive selection in the brainstem. These features of dispersion to the CNS are consistent with the action of selective processes, underlining the potential for H5N1 viruses to adapt to the CNS