Diatom Abundance and Diversity Across the Arcata Wastewater Treatment Plant and Wildlife Sanctuary

Wastewater management is an essential component of modern society that is necessary for reducing human environmental impact, particularly in aquatic ecosystems. In Humboldt County, California, the Arcata Wastewater Treatment Plant and Wildlife Sanctuary (Arcata Marsh) is a model for other wastewater treatment plants worldwide to treat waste naturally, reducing the use of chemicals. This wastewater is then discharged into the Humboldt Bay. It is well known how treatment helps remove harmful waste materials, but it has not been investigated how phytoplankton diversity is affected before, during, and after treatment. Phytoplankton are primary producers that are responsible for carbon sequestration and production of oxygen, and are an essential food source for higher trophic-level organisms. When nutrient levels are high, such as in human waste water, it can lead to single species proliferation, thus resulting in lower diversity and higher abundance of other species in the community. This can have negative consequences on the higher trophic levels that consume them and also creates “dead-zones\u27\u27 where aerobic species are unable to survive. In this study, pre-treatment water and post-treatment water were sampled and observed for diversity and abundance of diatoms, a quantifiable subphylum of phytoplankton. It was hypothesized that successful treatment would result in higher diversity of diatoms in post-treatment waters than that of pretreatment waters. This study found 30 morphologies across all sample sites, with abundance of 2-4 species being significantly greater in pre-treatment ponds than post-treatment ponds. There were no significant trends in diversity across the ponds

Moral economy from above and below: contesting contraction of migrant rights in austerity Britain

In 2010, Britain’s newly elected Coalition government ushered in a ‘moral mission’ of welfare reform. This paper considers its extension to the management of non-EEA migration and asylum, viewed here in the context of Fassin’s conception of moral economy and related debate. The paper argues that the ensuing policy regime can be analysed as a moral economy ‘from above’, in terms of its underlying objectives and rationale, which is then challenged and contested ‘from below’ through the intervention of civic activists. Such contestation is framed in terms of a three-pronged critique of the welfare/migration complex, based on rationality, legality and morality, and examined in three key areas of welfare-related policy change – family life, maintenance provision for asylum seekers, and support for those without status. Policy in each area is considered alongside corresponding critique and with summary comment on key points for moral economy analysis. A fourth section sets these developments in the context of an emergent system of total control, and the conclusion reflects on broader implications for our understanding and usage of the notion of moral economy

Truth, trust, and civic duty:Cultural factors in citizens' perceptions of mobile phone apps and social media in disasters

This study investigates how citizens perceive the role of mobile phone apps specifically designed for disaster communication, and how these perceptions may differ from perceived roles and functions of social media in disaster-related tasks/situations. Focusing on trust in authorities and technology use, results suggest that social media use not only fosters trust via shared narratives and collective sense-making but may also improve trust relationships through local authorities assuming the function of a trustworthy information provider. In disaster apps usage, trust between citizens and authorities is generated through perceptions of shared responsibility rather than shared narratives. Apps were seen as mechanisms that reveal authorities' general willingness to share control, which may help overcome citizens' perceptions that they are distrusted by authorities.</p

Determination whether the causal agent for mussel die-offs in the Mississippi River is of chemical or biological origin

ILENR Project 87/066Ope

Radial Construction of an Arterial Wall

SummarySome of the most serious diseases involve altered size and structure of the arterial wall. Elucidating how arterial walls are built could aid understanding of these diseases, but little is known about how concentric layers of muscle cells and the outer adventitial layer are assembled and patterned around endothelial tubes. Using histochemical, clonal, and genetic analysis in mice, here we show that the pulmonary artery wall is constructed radially, from the inside out, by two separate but coordinated processes. One is sequential induction of successive cell layers from surrounding mesenchyme. The other is controlled invasion of outer layers by inner layer cells through developmentally regulated cell reorientation and radial migration. We propose that a radial signal gradient controls these processes and provide evidence that PDGF-B and at least one other signal contribute. Modulation of such radial signaling pathways may underlie vessel-specific differences and pathological changes in arterial wall size and structure.Video Abstrac

Placental syncytiotrophoblast constitutes a major barrier to vertical transmission of Listeria monocytogenes.

Listeria monocytogenes is an important cause of maternal-fetal infections and serves as a model organism to study these important but poorly understood events. L. monocytogenes can infect non-phagocytic cells by two means: direct invasion and cell-to-cell spread. The relative contribution of each method to placental infection is controversial, as is the anatomical site of invasion. Here, we report for the first time the use of first trimester placental organ cultures to quantitatively analyze L. monocytogenes infection of the human placenta. Contrary to previous reports, we found that the syncytiotrophoblast, which constitutes most of the placental surface and is bathed in maternal blood, was highly resistant to L. monocytogenes infection by either internalin-mediated invasion or cell-to-cell spread. Instead, extravillous cytotrophoblasts-which anchor the placenta in the decidua (uterine lining) and abundantly express E-cadherin-served as the primary portal of entry for L. monocytogenes from both extracellular and intracellular compartments. Subsequent bacterial dissemination to the villous stroma, where fetal capillaries are found, was hampered by further cellular and histological barriers. Our study suggests the placenta has evolved multiple mechanisms to resist pathogen infection, especially from maternal blood. These findings provide a novel explanation why almost all placental pathogens have intracellular life cycles: they may need maternal cells to reach the decidua and infect the placenta

The mechanism of disaster capitalism and the failure to build community resilience:learning from the 2009 earthquake in L'Aquila, Italy

This paper reflects on what materialised during recovery operations following the earthquake in L'Aquila, Italy, on 6 April 2009. Previous critiques have focused on the actions of the Government of Italy and the Department of Civil Protection (Protezione Civile), with little attention paid to the role of local authorities. This analysis sheds light on how the latter used emergency powers, the command-and-control approach, and top-down planning to manage the disaster context, especially in terms of removal of rubble, implementing safety measures, and allocating temporary accommodation. It discusses how these arrangements constituted the mechanism via which ‘disaster capitalism’ took hold at the local and national level, and how it violated human rights, produced environmental and social impacts, hindered local communities from learning, transforming, and building resilience, and facilitated disaster capitalism and corruption. To make the disaster risk reduction and resilience paradigm more effective, a shift from centralised civil protection to decentralised, inclusive community empowerment systems is needed

Control of human endometrial stromal cell motility by PDGF-BB, HB-EGF and trophoblast-secreted factors

Human implantation involves extensive tissue remodeling at the fetal-maternal interface. It is becoming increasingly evident that not only trophoblast, but also decidualizing endometrial stromal cells are inherently motile and invasive, and likely contribute to the highly dynamic processes at the implantation site. The present study was undertaken to further characterize the mechanisms involved in the regulation of endometrial stromal cell motility and to identify trophoblast-derived factors that modulate migration. Among local growth factors known to be present at the time of implantation, heparin-binding epidermal growth factor-like growth factor (HB-EGF) triggered chemotaxis (directed locomotion), whereas platelet-derived growth factor (PDGF)-BB elicited both chemotaxis and chemokinesis (non-directed locomotion) of endometrial stromal cells. Supernatants of the trophoblast cell line AC-1M88 and of first trimester villous explant cultures stimulated chemotaxis but not chemokinesis. Proteome profiling for cytokines and angiogenesis factors revealed neither PDGF-BB nor HB-EGF in conditioned media from trophoblast cells or villous explants, while placental growth factor, vascular endothelial growth factor and PDGF-AA were identified as prominent secretory products. Among these, only PDGF-AA triggered endometrial stromal cell chemotaxis. Neutralization of PDGF-AA in trophoblast conditioned media, however, did not diminish chemoattractant activity, suggesting the presence of additional trophoblast-derived chemotactic factors. Pathway inhibitor studies revealed ERK1/2, PI3 kinase/Akt and p38 signaling as relevant for chemotactic motility, whereas chemokinesis depended primarily on PI3 kinase/Akt activation. Both chemotaxis and chemokinesis were stimulated upon inhibition of Rho-associated, coiled-coil containing protein kinase. The chemotactic response to trophoblast secretions was not blunted by inhibition of isolated signaling cascades, indicating activation of overlapping pathways in trophoblast-endometrial communication. In conclusion, trophoblast signals attract endometrial stromal cells, while PDGF-BB and HB-EGF, although not identified as trophoblast-derived, are local growth factors that may serve to fine-tune directed and non-directed migration at the implantation site

Expression of CD82 in Human Trophoblast and Its Role in Trophoblast Invasion

BACKGROUND: Well-controlled trophoblast invasion at maternal-fetal interface is a critical event for the normal development of placenta. CD82 is a member of transmembrane 4 superfamily, which showed important role in inhibiting tumor cell invasion and migration. We surmised that CD82 are participates in trophoblast differentiation during placenta development. METHODOLOGY/PRINCIPAL FINDINGS: CD82 was found to be strongly expressed in human first trimester placental villous and extravillous trophoblast cells as well as in trophoblast cell lines. To investigate whether CD82 plays a role in trophoblast invasion and migration, we further utilized human villous explants culture model on matrigel and invasion/migration assay of trophoblast cell line HTR8/SVneo. CD82 siRNA significantly promoted outgrowth of villous explants in vitro (P<0.01), as well as invasion and migration of HTR8/SVneo cells (P<0.05), whereas the trophoblast proliferation was not affected. The enhanced effect of CD82 siRNA on invasion and migration of trophoblast cells was found associated with increased gelatinolytic activities of matrix metalloproteinase MMP9 while over-expression of CD82 markedly decreased trphoblast cell invasion and migration as well as MMP9 activities. CONCLUSIONS/SIGNIFICANCE: These findings suggest that CD82 is an important negative regulator at maternal-fetal interface during early pregnancy, inhibiting human trophoblast invasion and migration