Effect of Groundwater Pumping on Seawater Intrusion in Coastal Aquifers

Many aquifers around the globe are located in coastal areas and are thus subjected to the seawater intrusion phenomenon. The growth of population in coastal areas and the conjugate increase in human, agricultural, and industrial activities have imposed an increasing demand for freshwater. This increase in water demand is often covered by extensive pumping of fresh groundwater, causing subsequent lowering of the water table (or piezometric head) and upsetting the dynamic balance between freshwater and saline water bodies. The classical result of such a development is seawater intrusion. This paper presents a review for the seawater intrusion phenomenon in coastal aquifers. The effect of pumping activities on the seawater intrusion in the Nile Delta aquifer of Egypt is investigated. It was concluded that any additional pumping should be located in the middle Delta and avoided in the eastern and western sides of the Delta

Rheumatoid synovial fluid interleukin-17-producing CD4 T cells have abundant tumor necrosis factor-alpha co-expression, but little interleukin-22 and interleukin-23R expression

Introduction\ud Th17 cells have been implicated in the pathogenesis of rheumatoid arthritis (RA). The aim of this study was to systematically analyse the phenotype, cytokine profile and frequency of interleukin-17 (IL-17) producing CD4-positive T cells in mononuclear cells isolated from peripheral blood, synovial fluid and synovial tissue of RA patients with established disease, and to correlate cell frequencies with disease activity. \ud \ud Methods\ud Flow cytometry was used to analyse the phenotype and cytokine production of mononuclear cells isolated from peripheral blood (PBMC) (n = 44), synovial fluid (SFMC) (n = 14) and synovium (SVMC) (n = 10) of RA patients and PBMC of healthy controls (n = 13). \ud \ud Results\ud The frequency of IL-17-producing CD4 T cells was elevated in RA SFMC compared with RA PBMC (P = 0.04). However, the frequency of this population in RA SVMC was comparable to that in paired RA PBMC. The percentage of IL-17-producing CD4 T cells coexpressing tumor necrosis factor alpha (TNFα) was significantly increased in SFMC (P = 0.0068). The frequency of IFNγ-producing CD4 T cells was also significantly higher in SFMC than paired PBMC (P = 0.042). The majority of IL-17-producing CD4 T cells coexpressed IFNγ. IL-17-producing CD4 T cells in RA PBMC and SFMC exhibited very little IL-22 or IL-23R coexpression. \ud \ud Conclusions\ud These findings demonstrate a modest enrichment of IL-17-producing CD4 T cells in RA SFMC compared to PBMC. Th17 cells in SFMC produce more TNFα than their PBMC counterparts, but are not a significant source of IL-22 and do not express IL-23R. However, the percentage of CD4 T cells which produce IL-17 in the rheumatoid joint is low, suggesting that other cells may be alternative sources of IL-17 within the joints of RA patients. \ud \u

Phoma stem canker disease on oilseed rape (Brassica napus) in China is caused by Leptosphaeria biglobosa ‘brassicae’

This document is the Accepted Manuscript version of the following article: Ze Liu, Akinwunmi O. Latunde-Dada, Avice M. Hall, Bruce D. L. Fitt, ‘Phoma stem canker disease on oilseed rape (Brassica napus) in China is caused by Leptosphaeria biglobosa ‘brassicae’’, European Journal of Plant Pathology, Vol. 140(4): 841-857, December 2014. The final publication is available at Springer via: http://dx.doi.org/10.1007/s10658-014-0513-7 © Koninklijke Nederlandse Planteziektenkundige Vereniging 2014Phoma stem canker of oilseed rape (Brassica napus) is a globally important disease that is caused by the sibling ascomycete species Leptosphaeria maculans and L. biglobosa. Sixty fungal isolates obtained from oilseed rape stems with phoma stem canker disease symptoms collected from four provinces in China in 1999, 2005 and 2006 were all identified as Leptosphaeria biglobosa, not L. maculans, by PCR diagnostics based on species-specific primers. There were no differences in cultural characteristics (e.g. pigmentation and in vitro growth) between these L. biglobosa isolates from China and those of 37 proven L. biglobosa isolates from Europe or Canada. In studies using amplified fragment length polymorphism (AFLP) markers, Chinese L. biglobosa populations were genetically more similar to European L. biglobosa populations than to the more diverse Canadian L. biglobosa populations. Sequencing of gene fragments of β-tubulin, actin and the internal transcribed spacer (ITS) region of rDNA from L. biglobosa isolates from China, Europe, Australia and Canada showed a closer taxonomic similarity of Chinese L. biglobosa to the European L. biglobosa ‘brassicae’ than to Canadian L. biglobosa ‘canadensis’ or to the Australian L. biglobosa ‘occiaustralensis’ or ‘australensis’ subclades. These results suggest that the Chinese L. biglobosa population in this study is in the same subclade as European L. biglobosa ‘brassicae’ populationsPeer reviewe

On the analysis of sedimentation velocity in the study of protein complexes

Sedimentation velocity analytical ultracentrifugation has experienced a significant transformation, precipitated by the possibility of efficiently fitting Lamm equation solutions to the experimental data. The precision of this approach depends on the ability to account for the imperfections of the experiment, both regarding the sample and the instrument. In the present work, we explore in more detail the relationship between the sedimentation process, its detection, and the model used in the mathematical data analysis. We focus on configurations that produce steep and fast-moving sedimentation boundaries, such as frequently encountered when studying large multi-protein complexes. First, as a computational tool facilitating the analysis of heterogeneous samples, we introduce the strategy of partial boundary modeling. It can simplify the modeling by restricting the direct boundary analysis to species with sedimentation coefficients in a predefined range. Next, we examine factors related to the experimental detection, including the magnitude of optical aberrations generated by out-of-focus solution columns at high protein concentrations, the relationship between the experimentally recorded signature of the meniscus and the meniscus parameter in the data analysis, and the consequences of the limited radial and temporal resolution of the absorbance optical scanning system. Surprisingly, we find that large errors can be caused by the finite scanning speed of the commercial absorbance optics, exceeding the statistical errors in the measured sedimentation coefficients by more than an order of magnitude. We describe how these effects can be computationally accounted for in SEDFIT and SEDPHAT

Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation

Background: Anoikis resistance is one of the abilities acquired along tumor progression. This characteristic is associated with metastasis development, since tumorigenic cells must survive independently of cell-matrix interactions in this process. in our laboratory, it was developed a murine melanocyte malignant transformation model associated with a sustained stressful condition. After subjecting melan-a melanocytes to 1, 2, 3 and 4 cycles of anchorage impediment, anoikis resistant cells were established and named 1C, 2C, 3C and 4C, respectively. These cells showed altered morphology and PMA independent cell growth, but were not tumorigenic, corresponding to pre-malignant cells. After limiting dilution of 4C pre-malignant cells, melanoma cell lines with different characteristics were obtained. Previous data from our group showed that increased Timp1 expression correlated with anoikis-resistant phenotype. Timp1 was shown to confer anchorage-independent growth capability to melan-a melanocytes and render melanoma cells more aggressive when injected into mice. However, the mechanisms involved in anoikis regulation by Timp1 in tumorigenic cells are not clear yet.Methods: the beta 1-integrin and Timp1 expression were evaluated by Western blotting and CD63 protein expression by flow cytometry using specific antibodies. To analyze the interaction among Timp1, CD63 and beta 1-integrin, immunoprecipitation assays were performed, anoikis resistance capability was evaluated in the presence or not of the PI3-K inhibitors, Wortmannin and LY294002. Relative expression of TIMP1 and CD63 in human metastatic melanoma cells was analyzed by real time PCR.Results: Differential association among Timp1, CD63 and beta 1-integrins was observed in melan-a melanocytes, 4C pre-malignant melanocytes and 4C11- and 4C11+ melanoma cells. Timp1 present in conditioned medium of melanoma cells rendered melan-a melanocytes anoikis-resistant through PI3-K signaling pathway independently of Akt activation. in human melanoma cell lines, in which TIMP1 and beta-1 integrin were also found to be interacting, TIMP1 and CD63 levels together was shown to correlate significantly with colony formation capacity.Conclusions: Our results show that Timp1 is assembled in a supramolecular complex containing CD63 and beta 1-integrins along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway, independently of Akt phosphorylation. in addition, our data point TIMP1, mainly together with CD63, as a potential biomarker of melanoma.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo, Dept Pharmacol, São Paulo, BrazilUniversidade Federal de São Paulo, Microbiol Immunol & Parasitol Dept, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, São Paulo, BrazilLudwig Inst Canc Res, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pharmacol, São Paulo, BrazilUniversidade Federal de São Paulo, Microbiol Immunol & Parasitol Dept, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, São Paulo, BrazilFAPESP: 2011/12306-1FAPESP: 2010/18715-8CAPES: 2867/10Web of Scienc

<em>Enterococcus faecalis</em> Infection Causes Inflammation, Intracellular Oxphos-Independent ROS Production, and DNA Damage in Human Gastric Cancer Cells

Background: Achlorhydria caused by e.g. atrophic gastritis allows for bacterial overgrowth, which induces chronic inflammation and damage to the mucosal cells of infected individuals driving gastric malignancies and cancer. Enterococcus faecalis (E. faecalis) can colonize achlohydric stomachs and we therefore wanted to study the impact of E. faecalis infection on inflammatory response, reactive oxygen species (ROS) formation, mitochondrial respiration, and mitochondrial genetic stability in gastric mucosal cells. Methods: To separate the changes induced by bacteria from those of the inflammatory cells we established an in vitro E. faecalis infection model system using the gastric carcinoma cell line MKN74. Total ROS and superoxide was measured by fluorescence microscopy. Cellular oxygen consumption was characterized non-invasively using XF24 microplate based respirometry. Gene expression was examined by microarray, and response pathways were identified by Gene Set Analysis (GSA). Selected gene transcripts were verified by quantitative real-time polymerase chain reaction (qRT-PCR). Mitochondrial mutations were determined by sequencing. Results: Infection of MKN74 cells with E. faecalis induced intracellular ROS production through a pathway independent of oxidative phosphorylation (oxphos). Furthermore, E. faecalis infection induced mitochondrial DNA instability. Following infection, genes coding for inflammatory response proteins were transcriptionally up-regulated while DNA damage repair and cell cycle control genes were down-regulated. Cell growth slowed down when infected with viable E. faecalis and responded in a dose dependent manner to E. faecalis lysate. Conclusions: Infection by E. faecalis induced an oxphos-independent intracellular ROS response and damaged the mitochondrial genome in gastric cell culture. Finally the bacteria induced an NF-kappa B inflammatory response as well as impaired DNA damage response and cell cycle control gene expression

Following REDD+: elite agendas, political temporalities, and the politics of environmental policy failure in Guyana

This article follows the journey of Guyana’s Reducing Emissions from Deforestation and Forest Degradation (REDD+) programme, from its promising emergence in 2009 as an ambitious, Norway-funded scheme worth US$250m to its near-abandonment by all actors ten years later. It is based on primary fieldwork conducted in Guyana in 2016 and 2017 and a deep review of the theoretical and empirical literature on REDD+ policy processes and the Norway–Guyana agreement. The article shows how, contrary to the mainstream understanding of environmental policy as a disinterested search for a rational, scientific solution, decisions governing REDD+ policy in Guyana were rather shaped throughout by the political objectives and calculations of a small number of opportunistic elite actors. It further shows how even the modest incarnation of REDD+ in Guyana (which ended up resembling more of a results-based aid programme than a Payment for Ecosystem Services scheme) was continually affected by political factors beyond the control of policy managers. These included fluctuations in the world gold price that led to an increase in mining activity and deforestation, the departure of a key international investor which caused the collapse of the flagship REDD+-funded Amaila Falls hydropower project, and legislative gridlock in Guyana generated by a hung Parliament. While not suggesting that REDD+ (or similar Payment for Ecosystem Services schemes) can never work, the article nonetheless illustrates the ways in which political objectives and unforeseen events can overwhelm substantive policy efforts towards fighting climate change. The findings also illustrate the dangers of prioritizing short-term ‘success stories’ over longer-term and more consultative environmental policy processes

Win-stay, lose-switch and public information strategies for patch fidelity of songbirds with rare extra-pair paternity

Determining where organisms breed and understanding why they breed in particular locations are fundamental biological questions with conservation implications. Breeding-site fidelity is common in migratory, territorial songbirds and is typically thought to occur following reproductive success with a social mate and success of nearby conspecifics. It is currently unknown if frequency of extra-pair paternity in a population influences use of information about reproductive success of nearby conspecifics for site fidelity decisions. We investigated patch fidelity of white-eyed vireos (Vireo griseus) based on reproductive success and quantified frequency of extra-pair paternity. We found support only for females making patch fidelity decisions following reproductive success with a social mate. Patch fidelity of males was not associated with reproductive success of nearby conspecifics, suggesting males may not use this information when extra-pair paternity is infrequent or the association is non-existent in this species