Seven-Year Results of Testing Paper Mill Residual Sludge as a Soil Ameliorant of Iron Mine Tailings

Paper mill residual solids, extracted from a settling pond in Newton Falls, NY, were tested for their efficacy as a site ameliorant. The test site was a twenty-five-year-old sand tailings, created by a former iron mining operation. Sludge was applied in trenches, as either 20% or 40% solids. Black locust, hybrid poplar, and willow seedlings were planted over the site to establish near forest-like vegetation. Seven years after establishment, overall survival is about 80%. The entrenched sludge provided increased soil moisture retention, deeper root development, increased nutrient availability and retention, and larger leaf sizes. Sludge applications resulted in greater above-ground height growth and greater root development for all species. Hybrid poplar cuttings exhibited the greatest rate of shoot development, while black locust seedlings exhibited the greatest rate of root development. The sludge application has produced a faster growing, more valuable ecosystem. This new artificial ecosystem has a greater variety of woody and herbaceous plants, higher fungi, and insects. It has a taller and more diverse vertical structure, contributing to increased wildlife habitat for at least some bird and mammal species

Activation of PKR by Bunyamwera virus is independent of the viral interferon antagonist NSs

Double-stranded RNA (dsRNA) is a by-product of viral RNA polymerase activity, and its recognition is one mechanism by which the innate immune system is activated. Cellular responses to dsRNA include induction of alpha/beta interferon (IFN) synthesis and activation of the enzyme PKR, which exerts its antiviral effect by phosphorylating the eukaryotic initiation factor eIF-2 alpha, thereby inhibiting translation. We have recently identified the nonstructural protein NSs of Bunyamwera virus (BUNV), the prototype of the family Bunyaviridae, as a virulence factor that blocks the induction of IFN by dsRNA. Here, we investigated the potential of NSs to inhibit PKR. We show that wild-type (wt) BUNV that expresses NSs triggered PKR-dependent phosphorylation of eIF-2 alpha to levels similar to those of a recombinant virus that does not express NSs (BUNdelNSs virus). Furthermore, the sensitivity of viruses in cell culture to IFN was independent of PKR and was not determined by NSs. PKR knockout mice, however, succumbed to infection approximately 1 day earlier than wt mice or mice deficient in expression of RNase L, another dsRNA-activated antiviral enzyme. Our data indicate that (i) bunyaviruses activate PKR, but are only marginally sensitive to its antiviral effect, and (ii) NSs is different from other IFN antagonists, since it inhibits dsRNA-dependent IFN induction but has no effect on the dsRNA-activated PKR and RNase L systems

Climate Crisis and Social Protection - From Worker Protection to Post-growth Transformation?

The article discusses five literature strands’ approaches towards social protection systems in the context of climate crisis: Adaptive Social Protection, Just Transition, Green New Deal, Post-growth, and Eco-feminism. As we argue, these five strands are located on a spectrum between a green growth orientation and a green anti-capitalist orientation. Furthermore, they differ in terms of their problematisation of the climate crisis and have different perspectives on relevant actors, on world regions, and – most relevant in the context of social welfare – their conceptualisation of social protection. While Adaptive Social Protection emphasizes cash transfers and insurances, Green New Deal and Just Transition approaches focus more on redistribution and labour market policies, and Post-growth and Eco-feminist approaches more on universalist policies and systems. We argue that these literatures each have their weaknesses, but also offer urgent questions, concepts, and insights for further social policy research

Schmallenberg virus pathogenesis, tropism and interaction with the innate immune system of the host

Schmallenberg virus (SBV) is an emerging orthobunyavirus of ruminants associated with outbreaks of congenital malformations in aborted and stillborn animals. Since its discovery in November 2011, SBV has spread very rapidly to many European countries. Here, we developed molecular and serological tools, and an experimental in vivo model as a platform to study SBV pathogenesis, tropism and virus-host cell interactions. Using a synthetic biology approach, we developed a reverse genetics system for the rapid rescue and genetic manipulation of SBV. We showed that SBV has a wide tropism in cell culture and “synthetic” SBV replicates in vitro as efficiently as wild type virus. We developed an experimental mouse model to study SBV infection and showed that this virus replicates abundantly in neurons where it causes cerebral malacia and vacuolation of the cerebral cortex. These virus-induced acute lesions are useful in understanding the progression from vacuolation to porencephaly and extensive tissue destruction, often observed in aborted lambs and calves in naturally occurring Schmallenberg cases. Indeed, we detected high levels of SBV antigens in the neurons of the gray matter of brain and spinal cord of naturally affected lambs and calves, suggesting that muscular hypoplasia observed in SBV-infected lambs is mostly secondary to central nervous system damage. Finally, we investigated the molecular determinants of SBV virulence. Interestingly, we found a biological SBV clone that after passage in cell culture displays increased virulence in mice. We also found that a SBV deletion mutant of the non-structural NSs protein (SBVΔNSs) is less virulent in mice than wild type SBV. Attenuation of SBV virulence depends on the inability of SBVΔNSs to block IFN synthesis in virus infected cells. In conclusion, this work provides a useful experimental framework to study the biology and pathogenesis of SBV

Novel coronavirus 2019-nCoV (COVID-19): early estimation of epidemiological parameters and epidemic size estimates

Since it was first identified, the epidemic scale of the recently emerged novel coronavirus (2019-nCoV) in Wuhan, China, has increased rapidly, with cases arising across China and other countries and regions. Using a transmission model, we estimate a basic reproductive number of 3.11 (95% CI, 2.39–4.13), indicating that 58–76% of transmissions must be prevented to stop increasing. We also estimate a case ascertainment rate in Wuhan of 5.0% (95% CI, 3.6–7.4). The true size of the epidemic may be significantly greater than the published case counts suggest, with our model estimating 21 022 (prediction interval, 11 090–33 490) total infections in Wuhan between 1 and 22 January. We discuss our findings in the light of more recent information. This article is part of the theme issue ‘Modelling that shaped the early COVID-19 pandemic response in the UK’

The British National Health Service 1948–2008: A Review of the Historiography

This article surveys historical writing on the British National Health Service since its inception in 1948. Its main focus is on policy-making and organisation and its principal concerns are primary care and the hospital sector, although public health, and psychiatric and geriatric care are briefly discussed. The over-arching narrative is one of transition from paternalism and technocratic planning to market disciplines and a discourse of choice, and of the ceding of professional autonomy by clinicians to managers and to the state. These issues are discussed in a chronological survey of policy-making from Bevan's ‘creation’ to the Blair era. Later sections consider evaluations of the service, starting with Webster's thesis that the NHS has been subject to prolonged under-funding, particularly under Conservative stewardship, then moving to assessments of the Thatcher, Major and Blair reforms. Much of the historical literature on the NHS is contentious and opinions are sharply divided on the reform era since the 1970s and the trajectories this has set for the future

Austerity, ageing and the financialisation of pensions policy in the UK

This article offers a detailed analysis of the recent history of pensions policy in the United Kingdom, culminating in two apparent ‘revolutions’ in policy now underway: the introduction of ‘automatic enrolment’ into private pensions, and proposals for a new ‘single-tier’ state pension. These reforms are considered exemplary of the ‘financialisation’ of UK welfare provision – typified in pensions policy by the notion that individuals must take personal responsibility for their own long-term financial security, and engage intimately with the financial services industry to do so. As such, the reforms represent the continuation of pensions policy between the Labour and coalition governments, despite the coalition government’s novel rhetorical commitment to austerity. In fact, the pensions revolutions will actually cost the state significantly more than current arrangements, yet the importance of fears about population ageing means that the government is both able to marshal the imagery of austerity to justify financialisation, but is also required to partly conceal the increased expenditure this requires. The article shows therefore how the financialisation agenda in pensions policy was evident before the financial crisis, but has evolved to both take advantage, and mitigate the constraints, of a post-crisis political climate

Generation and analysis of recombinant Bunyamwera orthobunyaviruses expressing V5 epitope-tagged L proteins

The L protein of Bunyamwera virus (BUNV; family Bunyaviridae) is an RNA-dependent RNA polymerase, 2238 aa in length, that catalyses transcription and replication of the negative-sense, tripartite RNA genome. To learn more about the molecular interactions of the L protein and to monitor its intracellular distribution we inserted a 14 aa V5 epitope derived from parainfluenza virus type 5, against which high-affinity antibodies are available, into different regions of the protein. Insertion of the epitope at positions 1935 or 2046 resulted in recombinant L proteins that retained functionality in a minireplicon assay. Two viable recombinant viruses, rBUNL4V5 and rBUNL5V5, expressing the tagged L protein were rescued by reverse genetics, and characterized with respect to their plaque size, growth kinetics and protein synthesis profile. The recombinant viruses behaved similarly to wild-type (wt) BUNV in BHK-21 cells, but formed smaller plaques and grew to lower titres in Vero E6 cells compared with wt BUNV. Immunofluorescent staining of infected cells showed the L protein to have a punctate to reticular distribution in the cytoplasm, and cell fractionation studies indicated that the L protein was present in both soluble and microsomal fractions. Co-immunoprecipitation and confocal microscopic assays confirmed an interaction between BUNV L and N proteins. The recombinant viruses expressing tagged L protein will be highly valuable reagents for the detailed dissection of the role of the BUNV L protein in virus replication

Inhibition of Interferon Induction and Action by the Nairovirus Nairobi Sheep Disease Virus/Ganjam Virus

The Nairoviruses are an important group of tick-borne viruses that includes pathogens of man (Crimean Congo hemorrhagic fever virus) and livestock animals (Dugbe virus, Nairobi sheep disease virus (NSDV)). NSDV is found in large parts of East Africa and the Indian subcontinent (where it is known as Ganjam virus). We have investigated the ability of NSDV to antagonise the induction and actions of interferon. Both pathogenic and apathogenic isolates could actively inhibit the induction of type 1 interferon, and also blocked the signalling pathways of both type 1 and type 2 interferons. Using transient expression of viral proteins or sections of viral proteins, these activities all mapped to the ovarian tumour-like protease domain (OTU) found in the viral RNA polymerase. Virus infection, or expression of this OTU domain in transfected cells, led to a great reduction in the incorporation of ubiquitin or ISG15 protein into host cell proteins. Point mutations in the OTU that inhibited the protease activity also prevented it from antagonising interferon induction and action. Interestingly, a mutation at a peripheral site, which had little apparent effect on the ability of the OTU to inhibit ubiquitination and ISG15ylation, removed the ability of the OTU to block the induction of type 1 and the action of type 2 interferons, but had a lesser effect on the ability to block type 1 interferon action, suggesting that targets other than ubiquitin and ISG15 may be involved in the actions of the viral OTU