Balancing macronutrient stoichiometry to alleviate eutrophication

Reactive nitrogen (N) and phosphorus (P) inputs to surface waters modify aquatic environments and affect public health and recreation. Until now, source control is the dominating measure of eutrophication management, and biological regulation of nutrients is largely neglected, although aquatic microbial organisms have huge potential to process nutrients. The stoichiometric ratio of organic carbon (OC) to N to P atoms should modulate heterotrophic pathways of aquatic nutrient processing, as high OC availability favours aquatic microbial processing. Such microbial processing removes N by denitrification and captures N and P as organically-complexed, less eutrophying forms. With a global data synthesis, we show that the atomic ratios of bioavailable dissolved OC to either N or P in rivers with urban and agricultural land use are often distant from a ‘microbial optimum’. This OC-deficiency relative to high availabilities of N and P likely overwhelms within-river heterotrophic processing and we propose that the capability of streams and rivers to retain N and P may be improved by active stoichiometric rebalancing. This rebalancing should be done by reconnecting appropriate OC sources such as wetlands and riparian forests, many of which have become disconnected from rivers concurrent to the progress of agriculture and urbanization. However, key knowledge gaps leave questions in the safe implementation of this approach in management: Mechanistic research is required to (i) evaluate system responses to catchment inputs of dissolved OC forms and amounts relative to internal-cycling controls of dissolved OC from aquatic production and particulate OC from aquatic and terrestrial sources and (ii) evaluate risk factors in anoxia-mediated P desorption with elevated OC scenarios. Still, we find this to be an approach with high potential for river management and we recommend to evaluate this stoichiometric approach for alleviating eutrophication, improving water quality and aquatic ecosystem health

Spongiibacter marinus gen. nov., sp. nov., a halophilic marine bacterium isolated from the boreal sponge Haliclona sp. 1

Strain HAL40bT was isolated from the marine sponge Haliclona sp. 1 collected at the Sula Ridge off the Norwegian coast and characterized by physiological, biochemical and phylogenetic analyses. The isolate was a small rod with a polar flagellum. It was aerobic, Gram-negative and oxidase- and catalase-positive. Optimal growth was observed at 20–30 °C, pH 7–9 and in 3 % NaCl. Substrate utilization tests were positive for arabinose, Tween 40 and Tween 80. Enzyme tests were positive for alkaline phosphatase, esterase lipase (C8), leucine arylamidase, acid phosphatase, naphthol-AS-BI-phosphohydrolase and N-acetyl-β-glucosaminidase. The predominant cellular fatty acid was C17 : 1 ω8, followed by C17 : 0 and C18 : 1 ω7. Analysis by matrix-assisted laser desorption/ionization time-of-flight MS was used to characterize the strain, producing a characteristic low-molecular-mass protein pattern that could be used as a fingerprint for identification of members of this species. The DNA G+C content was 69.1 mol%. Phylogenetic analysis supported by 16S rRNA gene sequence comparison classified the strain as a member of the class Gammaproteobacteria. Strain HAL40bT was only distantly related to other marine bacteria including Neptunomonas naphthovorans and Marinobacter daepoensis (type strain sequence similarity >90 %). Based on its phenotypic, physiological and phylogenetic characteristics, it is proposed that the strain should be placed into a new genus as a representative of a novel species, Spongiibacter marinus gen. nov., sp. nov.; the type strain of Spongiibacter marinus is HAL40bT (=DSM 17750T =CCUG 54896T)

Troubling stories of the end of occupy : feminist narratives of betrayal at occupy Glasgow

This article offers a feminist take on the question of why Occupy camps closed down, in the form of a narrative analysis of interviews from participants in Occupy Glasgow. In response to the emergence of an activist discourse emphasising the role of external forces in camp closure and the existence of a longer-term legacy in terms of individual and community politicisation, I build here on feminist interventions that point instead to serious internal problems within the camps and thus to a more limited legacy. Interrogating the plotting, characterisation and denouement of interviewee narratives, I show that feminist participants in Occupy Glasgow characterise the trajectory of the camp as a tragedy, attribute responsibility for the camp’s demise to co-campers and sometimes to themselves, and present the outcome of Occupy Glasgow as limited, and in some cases even traumatic. This raises serious questions about the culmination and outcomes of Occupy in Glasgow and more generally, and indicates the extent of the hard work remaining if future mobilisation against neoliberal austerity is to be more inclusive and sustainable. The article closes by considering the theoretical implications for the wider question of why movements come to an end

Tumor heterogeneity in VHL drives metastasis in clear cell renal cell carcinoma

Loss of function of the von Hippel-Lindau (VHL) tumor suppressor gene is a hallmark of clear cell renal cell carcinoma (ccRCC). The importance of heterogeneity in the loss of this tumor suppressor has been under reported. To study the impact of intratumoral VHL heterogeneity observed in human ccRCC, we engineered VHL gene deletion in four RCC models, including a new primary tumor cell line derived from an aggressive metastatic case. The VHL gene-deleted (VHL-KO) cells underwent epithelial-to-mesenchymal transition (EMT) and exhibited increased motility but diminished proliferation and tumorigenicity compared to the parental VHL-expressing (VHL+) cells. Renal tumors with either VHL+ or VHL-KO cells alone exhibit minimal metastatic potential. Combined tumors displayed rampant lung metastases, highlighting a novel cooperative metastatic mechanism. The poorly proliferative VHL-KO cells stimulated the proliferation, EMT, and motility of neighboring VHL+ cells. Periostin (POSTN), a soluble protein overexpressed and secreted by VHL non-expressing (VHL-) cells, promoted metastasis by enhancing the motility of VHL-WT cells and facilitating tumor cell vascular escape. Genetic deletion or antibody blockade of POSTN dramatically suppressed lung metastases in our preclinical models. This work supports a new strategy to halt the progression of ccRCC by disrupting the critical metastatic crosstalk between heterogeneous cell populations within a tumor

Reciprocity as a foundation of financial economics

This paper argues that the subsistence of the fundamental theorem of contemporary financial mathematics is the ethical concept ‘reciprocity’. The argument is based on identifying an equivalence between the contemporary, and ostensibly ‘value neutral’, Fundamental Theory of Asset Pricing with theories of mathematical probability that emerged in the seventeenth century in the context of the ethical assessment of commercial contracts in a framework of Aristotelian ethics. This observation, the main claim of the paper, is justified on the basis of results from the Ultimatum Game and is analysed within a framework of Pragmatic philosophy. The analysis leads to the explanatory hypothesis that markets are centres of communicative action with reciprocity as a rule of discourse. The purpose of the paper is to reorientate financial economics to emphasise the objectives of cooperation and social cohesion and to this end, we offer specific policy advice

[Introduction] Toward an anthropology of the just price: history, ethnography, critique

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Towards a pathway definition of Parkinson’s disease: a complex disorder with links to cancer, diabetes and inflammation

We have previously established a first whole genome transcriptomic profile of sporadic Parkinson’s disease (PD). After extensive brain tissue-based validation combined with cycles of iterative data analysis and by focusing on the most comparable cases of the cohort, we have refined our analysis and established a list of 892 highly dysregulated priority genes that are considered to form the core of the diseased Parkinsonian metabolic network. The substantia nigra pathways, now under scrutiny, contain more than 100 genes whose association with PD is known from the literature. Of those, more than 40 genes belong to the highly significantly dysregulated group identified in our dataset. Apart from the complete list of 892 priority genes, we present pathways revealing PD ‘hub’ as well as ‘peripheral’ network genes. The latter include Lewy body components or interact with known PD genes. Biological associations of PD with cancer, diabetes and inflammation are discussed and interactions of the priority genes with several drugs are provided. Our study illustrates the value of rigorous clinico-pathological correlation when analysing high-throughput data to make optimal use of the histopathological phenome, or morphonome which currently serves as the key diagnostic reference for most human diseases. The need for systematic human tissue banking, following the highest possible professional and ethical standard to enable sustainability, becomes evident

Hypoxia regulates human lung fibroblast proliferation via p53-dependent and -independent pathways

<p>Abstract</p> <p>Background</p> <p>Hypoxia induces the proliferation of lung fibroblasts in vivo and in vitro. However, the subcellular interactions between hypoxia and expression of tumor suppressor p53 and cyclin-dependent kinase inhibitors p21 and p27 remain unclear.</p> <p>Methods</p> <p>Normal human lung fibroblasts (NHLF) were cultured in a hypoxic chamber or exposed to desferroxamine (DFX). DNA synthesis was measured using bromodeoxyuridine incorporation, and expression of p53, p21 and p27 was measured using real-time RT-PCR and Western blot analysis.</p> <p>Results</p> <p>DNA synthesis was increased by moderate hypoxia (2% oxygen) but was decreased by severe hypoxia (0.1% oxygen) and DFX. Moderate hypoxia decreased p21 synthesis without affecting p53 synthesis, whereas severe hypoxia and DFX increased synthesis of both p21 and p53. p27 protein expression was decreased by severe hypoxia and DFX. Gene silencing of p21 and p27 promoted DNA synthesis at ambient oxygen concentrations. p21 and p53 gene silencing lessened the decrease in DNA synthesis due to severe hypoxia or DFX exposure. p21 gene silencing prevented increased DNA synthesis in moderate hypoxia. p27 protein expression was significantly increased by p53 gene silencing, and was decreased by wild-type p53 gene transfection.</p> <p>Conclusion</p> <p>These results indicate that in NHLF, severe hypoxia leads to cell cycle arrest via the p53-p21 pathway, but that moderate hypoxia enhances cell proliferation via the p21 pathway in a p53-independent manner. In addition, our results suggest that p27 may be involved in compensating for p53 in cultured NHLF proliferation.</p