The Effect of Natural Dissolved Organic Carbon on the Acute Toxicity of Copper to Larval Freshwater Mussels (\u3cem\u3eGlochidia\u3c/em\u3e)

The present study examined the effect of dissolved organic carbon (DOC), both added and inherent, on Cu toxicity in glochidia, the larvae of freshwater mussels. Using incremental additions of natural DOC concentrate and reconstituted water, a series of acute copper toxicity tests were conducted. An increase in DOC from 0.7 to 4.4 mg C/L resulted in a fourfold increase (36–150 μg Cu/L) in the 24-h median effective concentration (EC50) and a significant linear relationship (r2=0.98, p=0.0008) between the DOC concentration and the Cu EC50 of Lampsilis siliquoidea glochidia. The ameliorating effect of added DOC on Cu toxicity was confirmed using a second mussel species, the endangered (in Canada) Lampsilis fasciola. The effect of inherent (i.e., not added) DOC on Cu toxicity was also assessed in eight natural waters (DOC 5–15 mg C/L). These experiments revealed a significant relationship between the EC50 and the concentration of inherent DOC (r2=0.79, p=0.0031) with EC50s ranging from 27 to 111 μg Cu/L. These laboratory tests have demonstrated that DOC provides glochidia with significant protection from acute Cu toxicity. The potential risk that Cu poses to mussel populations was assessed by comparing Cu and DOC concentrations from significant mussel habitats in Ontario to the EC50s. Although overall mean Cu concentration in the mussel’s habitat was well below the acutely toxic level given the concentration of DOC, episodic Cu releases in low DOC waters may be a concern for the recovery of endangered freshwater mussels. The results are examined in the context of current Cu water quality regulations including the U.S. Environmental Protection Agency’s (U.S. EPA) biotic ligand model

Physiological Responses to Acute Silver Exposure in the Freshwater Crayfish (\u3cem\u3eCambarus diogenes diogenes\u3c/em\u3e)—A Model Invertebrate?

Adult crayfish (Cambarus diogenes diogenes) exposed to 8.41 ± 0.17 μg silver/L (19.4% as Ag+) in moderately hard freshwater under flow-through conditions for 96 h exhibited ionoregulatory disturbance, elevated metabolic ammonia (Tamm) production and substantial silver accumulation in the gills, hemolymph, and hepatopancreas. The ionoregulatory disturbance included both a generally reduced unidirectional Na1 influx and an increased unidirectional Na+ efflux, leading to a substantial net loss of Na+ from the silver-exposed crayfish. The Na+ uptake in silver-exposed crayfish differed overall from controls, while the increased Na+ efflux recovered to control values 48 h into the 96 h of exposure. The general inhibition of Na+ uptake could be explained by a reduced sodium/potassium-adenosine triphosphatase (Na/K-ATPase) activity in terminally obtained gill samples from the silver exposed crayfish. The silver-induced effect on Na+ uptake and loss translated to reduced hemolymph Na+ concentrations but not significantly reduced hemolymph Cl- concentrations. Hemolymph Tamm and Tamm efflux both increased in silver-exposed crayfish, indicating an increased metabolic Tamm production. The present study demonstrates that the toxic mechanism of waterborne silver exposure in freshwater crayfish resembles that of freshwater teleost fish. The crayfish might therefore be a useful model system for extending current environmental regulatory strategies, currently based on teleost fish, to invertebrates

South Africa - CGIAR Partnership Results in New Maize Varieties with 30 to 50 percent higher yields

TB

Arrive, survive and thrive: essential stages in the re-colonization and recovery of zooplankton in urban lakes in Sudbury, Canada

The recovery of lakes from severe, historical acid and metal pollution requires that colonists of extirpated species arrive, survive and subsequently thrive. We employed 40 year records from weekly to monthly crustacean zooplankton samples from Middle and Clearwater lakes near Sudbury, Canada, to identify the main mechanistic bottlenecks in this recovery process. While both lakes now have circum-neutral pH, acidity decreased more rapidly in Middle Lake because of past liming interventions, while Clearwater Lake, being larger and supporting more housing, likely receives more zooplankton colonists than Middle Lake. Community richness increased much faster in Middle Lake than in Clearwater Lake, at 1.6 vs 0.9 species decade-1, respectively. Richness has recovered in Middle Lake, when assessed against a target of 9-16 species collection-1 determined from regional reference lakes, but it has not yet recovered in Clearwater Lake. Species accumulation curves and a metric of annual persistence show that this difference is a product not of greater rates of species introduction into Middle Lake, but rather to their greater annual persistence once introduced. Greater annual persistence was associated with better habitat quality (i.e., lower acid and metal toxicity) in Middle Lake, particularly early in the record, and lower planktivore abundance, more recently. These results support a growing consensus that ecological recovery of zooplankton from acidification and metal pollution does not depend strongly on propagule introduction rates which are adequate, but rather on propagule persistence, in lake-rich, suburban landscapes such as those near Sudbury

IFN-γ signaling, with the synergistic contribution of TNF-α, mediates cell specific microglial and astroglial activation in experimental models of Parkinson's disease

To through light on the mechanisms underlying the stimulation and persistence of glial cell activation in Parkinsonism, we investigate the function of IFN-γ and TNF-α in experimental models of Parkinson's disease and analyze their relation with local glial cell activation. It was found that IFN-γ and TNF-α remained higher over the years in the serum and CNS of chronic Parkinsonian macaques than in untreated animals, accompanied by sustained glial activation (microglia and astroglia) in the substantia nigra pars compacta. Importantly, Parkinsonian monkeys showed persistent and increasing levels of IFN-γR signaling in both microglial and astroglial cells. In addition, experiments performed in IFN-γ and TNF-α KO mice treated with MPTP revealed that, even before dopaminergic cell death can be observed, the presence of IFN-γ and TNF-α is crucial for microglial and astroglial activation, and, together, they have an important synergistic role. Both cytokines were necessary for the full level of activation to be attained in both microglial and astroglial cells. These results demonstrate that IFN-γ signaling, together with the contribution of TNF-α, have a critical and cell-specific role in stimulating and maintaining glial cell activation in Parkinsonism

Philosophy of Hope

The philosophy of hope centers on two interlocking sets of questions. The first concerns the nature of hope. Specific questions here include how to analyze hope, how hope motivates us, and whether there is only one type of hope. The second set concerns the value of hope. Key questions here include whether and when it is good to hope and whether there is a virtue of hope. Philosophers of hope tend to proceed from the first set of questions to the second. This is a natural approach, for one might expect that you must develop a basic understanding of what hope is before you can determine its value. The structure of this chapter thus follows this approach. But readers should not be misled: there is in fact a good deal of feedback between the two sets of questions. A theory of hope is more plausible to the extent that it fits well with plausible ideas about the value of hope. So the movement from hope’s nature to its value is one of emphasis rather than a strict, step-wise process

Epidemiology of influenza-associated hospitalization in adults, Toronto, 2007/8

The purpose of this investigation was to identify when diagnostic testing and empirical antiviral therapy should be considered for adult patients requiring hospitalization during influenza seasons. During the 2007/8 influenza season, six acute care hospitals in the Greater Toronto Area participated in active surveillance for laboratory-confirmed influenza requiring hospitalization. Nasopharyngeal (NP) swabs were obtained from patients presenting with acute respiratory or cardiac illness, or with febrile illness without clear non-respiratory etiology. Predictors of influenza were analyzed by multivariable logistic regression analysis and likelihoods of influenza infection in various patient groups were calculated. Two hundred and eighty of 3,917 patients were found to have influenza. Thirty-five percent of patients with influenza presented with a triage temperature ≥38.0°C, 80% had respiratory symptoms in the emergency department, and 76% were ≥65 years old. Multivariable analysis revealed a triage temperature ≥38.0°C (odds ratio [OR] 3.1; 95% confidence interval [CI] 2.3–4.1), the presence of respiratory symptoms (OR 1.7; 95% CI 1.2–2.4), admission diagnosis of respiratory infection (OR 1.8; 95% CI 1.3–2.4), admission diagnosis of exacerbation of chronic obstructive pulmonary disease (COPD)/asthma or respiratory failure (OR 2.3; 95% CI 1.6–3.4), and admission in peak influenza weeks (OR 4.2; 95% CI 3.1–5.7) as independent predictors of influenza. The likelihood of influenza exceeded 15% in patients with respiratory infection or exacerbation of COPD/asthma if the triage temperature was ≥38.0°C or if they were admitted in the peak weeks during the influenza season. During influenza season, diagnostic testing and empiric antiviral therapy should be considered in patients requiring hospitalization if respiratory infection or exacerbation of COPD/asthma are suspected and if either the triage temperature is ≥38.0°C or admission is during the weeks of peak influenza activity

When should a diagnosis of influenza be considered in adults requiring intensive care unit admission? Results of population-based active surveillance in Toronto

INTRODUCTION: There is a paucity of data about the clinical characteristics that help identify patients at high risk of influenza infection upon ICU admission. We aimed to identify predictors of influenza infection in patients admitted to ICUs during the 2007/2008 and 2008/2009 influenza seasons and the second wave of the 2009 H1N1 influenza pandemic as well as to identify populations with increased likelihood of seasonal and pandemic 2009 influenza (pH1N1) infection. METHODS: Six Toronto acute care hospitals participated in active surveillance for laboratory-confirmed influenza requiring ICU admission during periods of influenza activity from 2007 to 2009. Nasopharyngeal swabs were obtained from patients who presented to our hospitals with acute respiratory or cardiac illness or febrile illness without a clear nonrespiratory aetiology. Predictors of influenza were assessed by multivariable logistic regression analysis and the likelihood of influenza in different populations was calculated. RESULTS: In 5,482 patients, 126 (2.3%) were found to have influenza. Admission temperature ≥38°C (odds ratio (OR) 4.7 for pH1N1, 2.3 for seasonal influenza) and admission diagnosis of pneumonia or respiratory infection (OR 7.3 for pH1N1, 4.2 for seasonal influenza) were independent predictors for influenza. During the peak weeks of influenza seasons, 17% of afebrile patients and 27% of febrile patients with pneumonia or respiratory infection had influenza. During the second wave of the 2009 pandemic, 26% of afebrile patients and 70% of febrile patients with pneumonia or respiratory infection had influenza. CONCLUSIONS: The findings of our study may assist clinicians in decision making regarding optimal management of adult patients admitted to ICUs during future influenza seasons. Influenza testing, empiric antiviral therapy and empiric infection control precautions should be considered in those patients who are admitted during influenza season with a diagnosis of pneumonia or respiratory infection and are either febrile or admitted during weeks of peak influenza activity

Moving Stories: Agency, Emotion and Practical Rationality

What is it to be an agent? One influential line of thought, endorsed by G. E. M. Anscombe and David Velleman, among others, holds that agency depends on practical rationality—the ability to act for reasons, rather than being merely moved by causes. Over the past 25 years, Velleman has argued compellingly for a distinctive view of agency and the practical rationality with which he associates it. On Velleman’s conception, being an agent consists in having the capacity to be motivated by a drive to act for reasons. Your bodily movements qualify as genuine actions insofar as they are motivated in part by your desire to behave in a way that makes sense to yourself. However, there are at least two distinct ways of spelling out what this drive towards self-intelligibility consists in, both present in Velleman’s work. It might consist in a drive towards intelligibility in causal-psychological terms: roughly, a drive to maximize the rational coherence of your psychological states. Alternatively, it might consist in a drive towards narrative intelligibility: a drive to make your ongoing activity conform to a recognizable narrative structure, where that structure is understood emotionally. Velleman originally saw these options as basically equivalent, but later came to prioritize the drive towards causal-psychological intelligibility over that towards narrative intelligibility. I argue that this gets things the wrong way round—we should instead understand our capacities to render ourselves intelligible in causal-psychological terms as built upon a bedrock of emotionally suffused narrative understanding. In doing so, we resolve several problems for Velleman’s view, and pave the way for an embodied, embedded and affective account of practical rationality and agency. According to the picture that emerges, practical rationality is essential to agency, narrative understanding is essential to practical rationality, and the rhythms and structures patterning the ebb and flow of our emotional lives are essential to narrative understanding

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions