92 research outputs found

    Algal blooms and the nitrogen-enrichment hypothesis in Florida springs: evidence, alternatives, and adaptive management.

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    Contradictions between system-specific evidence and broader paradigms to explain ecosystem behavior present a challenge for natural resource management. In Florida (U.S.A.) springs, increasing nitrate (NO3-) concentrations have been implicated as the cause of algal overgrowth via alleviation of N-limitation. As such, policy and management efforts have centered heavily on reduction of nitrogen (N) loads. While the N-limitation hypothesis appears well founded on broadly supported aquatic eutrophication models, several observations from Florida springs are inconsistent with this hypothesis in its present simplified form. First, NO3- concentration is not correlated with algal abundance across the broad population of springs and is weakly negatively correlated with primary productivity. Second, within individual spring runs, algal mats are largely confined to the headwater reaches within 250 m of spring vents, while elevated NO3- concentrations persist for several kilometers or more. Third, historic observations suggest that establishment of macroalgal mats often lags behind observed increases in NO3- by more than a decade. Fourth, although microcosm experiments indicate high thresholds for N-limitation of algae, experiments in situ have demonstrated only minimal response to N enrichment. These muted responses may reflect large nutrient fluxes in springs, which were sufficient to satisfy present demand even at historic concentrations. New analyses of existing data indicate that dissolved oxygen (DO) has declined dramatically in many Florida springs over the past 30 years, and that DO and grazer abundance are better predictors of algal abundance in springs than are nutrient concentrations. Although a precautionary N-reduction strategy for Florida springs is warranted given demonstrable effects of nutrient enrichment in a broad suite of aquatic systems worldwide, the DO-grazer hypothesis and other potential mechanisms merit increased scientific scrutiny. This case study illustrates the importance of an adaptive approach that explicitly evaluates paradigms as hypotheses and actively seeks alternative explanations

    Microarray identifies ADAM family members as key responders to TGF-β1 in alveolar epithelial cells

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    The molecular mechanisms of Idiopathic Pulmonary Fibrosis (IPF) remain elusive. Transforming Growth Factor beta 1(TGF-β1) is a key effector cytokine in the development of lung fibrosis. We used microarray and computational biology strategies to identify genes whose expression is significantly altered in alveolar epithelial cells (A549) in response to TGF-β1, IL-4 and IL-13 and Epstein Barr virus. A549 cells were exposed to 10 ng/ml TGF-β1, IL-4 and IL-13 at serial time points. Total RNA was used for hybridisation to Affymetrix Human Genome U133A microarrays. Each in vitro time-point was studied in duplicate and an average RMA value computed. Expression data for each time point was compared to control and a signal log ratio of 0.6 or greater taken to identify significant differential regulation. Using normalised RMA values and unsupervised Average Linkage Hierarchical Cluster Analysis, a list of 312 extracellular matrix (ECM) proteins or modulators of matrix turnover was curated via Onto-Compare and Gene-Ontology (GO) databases for baited cluster analysis of ECM associated genes. Interrogation of the dataset using ontological classification focused cluster analysis revealed coordinate differential expression of a large cohort of extracellular matrix associated genes. Of this grouping members of the ADAM (A disintegrin and Metalloproteinase domain containing) family of genes were differentially expressed. ADAM gene expression was also identified in EBV infected A549 cells as well as IL-13 and IL-4 stimulated cells. We probed pathologenomic activities (activation and functional activity) of ADAM19 and ADAMTS9 using siRNA and collagen assays. Knockdown of these genes resulted in diminished production of collagen in A549 cells exposed to TGF-β1, suggesting a potential role for these molecules in ECM accumulation in IPF

    Change in quality of life and their predictors in the long-term follow-up after group cognitive behavioral therapy for social anxiety disorder: a prospective cohort study

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    <p>Abstract</p> <p>Background</p> <p>Social anxiety disorder (SAD) is one of the most common anxiety disorders. The efficacy of cognitive behaviour therapy (CBT) has been examined but to date its effects on Quality of Life (QoL) have not been appropriately evaluated especially in the long term.</p> <p>The study aimed to examine, in the long term, what aspects of Quality of Life (QoL) changed among social anxiety disorder (SAD) patients treated with group cognitive behaviour therapy (CBT) and what predictors at baseline were associated with QoL.</p> <p>Methods</p> <p>Outpatients diagnosed with SAD were enrolled into group CBT, and assessed at follow-ups for up to 12 months in a typical clinical setting. QoL was evaluated using the Short Form 36. Various aspects of SAD symptomatology were also assessed. Each of the QoL domains and scores on symptomatology were quantified and compared with those at baseline. Baseline predictors of QoL outcomes at follow-up were investigated.</p> <p>Results</p> <p>Fifty-seven outpatients were enrolled into group CBT for SAD, 48 completed the whole program, and 44 and 40 completed assessments at the 3-month and 12-month follow-ups, respectively. All aspects of SAD symptomatology and psychological subscales of the QoL showed statistically significant improvement throughout follow-ups for up to 12 months. In terms of social functioning, no statistically significant improvement was observed at either follow-up point except for post-treatment. No consistently significant pre-treatment predictors were observed.</p> <p>Conclusions</p> <p>After group CBT, SAD symptomatology and some aspects of QoL improved and this improvement was maintained for up to 12 months, but the social functioning domain did not prove any significant change statistically. Considering the limited effects of CBT on QoL, especially for social functioning, more powerful treatments are needed.</p

    Altered Effective Connectivity Network of the Amygdala in Social Anxiety Disorder: A Resting-State fMRI Study

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    The amygdala is often found to be abnormally recruited in social anxiety disorder (SAD) patients. The question whether amygdala activation is primarily abnormal and affects other brain systems or whether it responds “normally” to an abnormal pattern of information conveyed by other brain structures remained unanswered. To address this question, we investigated a network of effective connectivity associated with the amygdala using Granger causality analysis on resting-state functional MRI data of 22 SAD patients and 21 healthy controls (HC). Implications of abnormal effective connectivity and clinical severity were investigated using the Liebowitz Social Anxiety Scale (LSAS). Decreased influence from inferior temporal gyrus (ITG) to amygdala was found in SAD, while bidirectional influences between amygdala and visual cortices were increased compared to HCs. Clinical relevance of decreased effective connectivity from ITG to amygdala was suggested by a negative correlation of LSAS avoidance scores and the value of Granger causality. Our study is the first to reveal a network of abnormal effective connectivity of core structures in SAD. This is in support of a disregulation in predescribed modules involved in affect control. The amygdala is placed in a central position of dysfunction characterized both by decreased regulatory influence of orbitofrontal cortex and increased crosstalk with visual cortex. The model which is proposed based on our results lends neurobiological support towards cognitive models considering disinhibition and an attentional bias towards negative stimuli as a core feature of the disorder

    A Guide to Medications Inducing Salivary Gland Dysfunction, Xerostomia, and Subjective Sialorrhea: A Systematic Review Sponsored by the World Workshop on Oral Medicine VI

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