Teaching across disciplines: a case study of a project-based short course to teach holistic coastal adaptation design

Climate change has led to the need for innovation in resilient infrastructure and the social policies which will support those. This requires greater interdisciplinary interactions and knowledge building among emerging professionals. This paper presents a case study of a pilot short course intended to immerse graduate students in the design of resilient infrastructure using place-based and interdisciplinary active team learning. This course helps graduate students bridge the gap between research and practice on the social science and engineering of resilient infrastructure for coastal adaptation. The intellectual framework for the course (the Adaptive Gradients Framework) provides a holistic evaluation of adaptation design proposals and was used to recognize the complexity of social, ecological and engineering aspects and varied social benefits. The course provides a model to move outside rigid boundaries of institutions and disciplines to begin to build, in both students and instructors, the ability to work more effectively on complex social-ecological-engineering problems. Finally, this paper presents a summary of lessons learned from this pilot short course

Effect of thermal phase fluctuations on the superfluid density of two-dimensional superconducting films

High precision measurements of the complex sheet conductivity of superconducting Mo77Ge23 thin films have been made from 0.4 K through Tc. A sharp drop in the inverse sheet inductance, 1/L(T), is observed at a temperature, Tc, which lies below the mean-field transition temperature, Tco. Just below Tc, the suppression of 1/L(T) below its mean-field value indicates that longitudinal phase fluctuations have nearly their full classical amplitude, but they disappear rapidly as T decreases. We argue that there is a quantum crossover at about 0.94 Tco, below which classical phase fluctuations are suppressed.Comment: 14 pages, 3 figures. Subm. to PR

On religion and cultural policy: notes on the Roman Catholic Church

This paper argues that religious institutions have largely been neglected within the study of cultural policy. This is attributed to the inherently secular tendency of most modern social sciences. Despite the predominance of the ‘secularisation paradigm’, the paper notes that religion continues to promote powerful attachments and denunciations. Arguments between the ‘new atheists’, in particular, Richard Dawkins, and their opponents are discussed, as is Habermas’s conciliatory encounter with Joseph Ratzinger (later Pope Benedict XVI). The paper then moves to a consideration of the Roman Catholic Church as an agent of cultural policy, whose overriding aim is the promotion of ‘Christian consciousness’. Discussion focuses on the contested meanings of this, with reference to (1) the deliberations of Vatican II and (2) the exercise of theological and cultural authority by the Pope and the Congregation for the Doctrine of the Faith (CDF). It is argued that these doctrinal disputes intersect with secular notions of social and cultural policy and warrant attention outside the specialist realm of theological discourse

A review of climate change and the implementation of marine biodiversity legislation in the United Kingdom

1. Marine legislation, the key means by which the conservation of marine biodiversity is achieved, has been developing since the 1960s. In recent decades, an increasing focus on ‘holistic’ policy development is evident, compared with earlier ‘piecemeal’ sectoral approaches. Important marine legislative tools being used in the United Kingdom, and internationally, include the designation of marine protected areas and the Marine Strategy Framework Directive (MSFD) with its aim of meeting ‘Good Environmental Status’ (GES) for European seas by 2020. 2. There is growing evidence of climate change impacts on marine biodiversity, which may compromise the effectiveness of any legislation intended to promote sustainable marine resource management. 3. A review of key marine biodiversity legislation relevant to the UK shows climate change was not considered in the drafting of much early legislation. Despite the huge increase in knowledge of climate change impacts in recent decades, legislation is still limited in how it takes these impacts into account. There is scope, however, to account for climate change in implementing much of the legislation through (a) existing references to environmental variability; (b) review cycles; and (c) secondary legislation and complementary policy development. 4. For legislation relating to marine protected areas (e.g. the EC Habitats and Birds Directives), climate change has generally not been considered in the site-designation process, or for ongoing management, with the exception of the Marine (Scotland) Act. Given that changing environmental conditions (e.g. rising temperatures and ocean acidification) directly affect the habitats and species that sites are designated for, how this legislation is used to protect marine biodiversity in a changing climate requires further consideration. 5. Accounting for climate change impacts on marine biodiversity in the development and implementation of legislation is vital to enable timely, adaptive management responses. Marine modelling can play an important role in informing management decisions

A critical review of the formation of mono- and dicarboxylated metabolic intermediates of alkylphenol polyethoxylates during wastewater treatment and their environmental significance

This is the author's accepted manuscript. The final published article is available from the link below. Copyright @ 2010 Taylor & Francis.Alkylphenoxyacetic acids, the metabolic biodegradation products of alkylphenol ethoxylates, are commonly found in wastewaters and sewage effluents. These persistent hydrophilic derivatives possess intrinsic estrogenic activity, which can mimic natural hormones. Their concentrations increase through the sewage treatment works as a result of biodegradation and biotransformation, and when discharged can disrupt endocrine function in fish. These acidic metabolites represent the dominant alkylphenolic compounds found in wastewater effluent and their presence is cause for concern as, potentially, through further biotransformation and biodegradation, they can act as sources of nonylphenol, which is toxic and estrogenic. The authors aim to assess the mechanisms of formation as well as elimination of alkylphenoxyacetic acids within conventional sewage treatment works with the emphasis on the activated sludge process. In addition, they evaluate the various factors influencing their degradation and formation in laboratory scale and full-scale systems. The environmental implications of these compounds are considered, as is the need for tertiary treatment processes for their removal

Use of a differential pressure transducer for the monitoring of soil volume change in cyclic triaxial test on unsaturated soils

A new experimental set-up using a differential pressure transducer was developed, that enables the monitoring of volume changes in cyclic triaxial tests on unsaturated soils. Calibration tests were performed in order to analyze the performance of the set-up, especially in terms of loading frequencies. Based on calibration results, a low frequency of 0.05 Hz was adopted for the tests carried out on the unsaturated loess from northern France. Five water contents were considered in the tests. The obtained results have confirmed the efficiency of the new system for volume change monitoring under cyclic loading. The effect of water content on the cyclic behavior of loess was clearly evidenced. Finally, some suggestions were made to improve the accuracy of the system

Using high resolution digital aerial imagery interpreted in a 3-D digital GIS environment to map predefined plant communities in central-southern New South Wales

Aerial photo interpretation of high resolution airborne imagery (ADS40) was used in a three-dimensional (3-D) digital Geographic Information System (GIS) environment to map native plant communities defined in the NSW Vegetation Classification and Assessment (NSW VCA) in central-southern New South Wales. NSW VCA plant community types form part of the NSW BioMetric vegetation type dataset underpinning NSW natural resource management (NRM) planning frameworks. This region was previously devoid of detailed vegetation mapping. In addition to developing a novel method for mapping plant communities, the use of ADS40 imagery allowed for capture of multiple attributes in each map polygon including attributes pertaining to dominant species and vegetation condition. Such data informs multi-attribute models used in conservation planning, providing utility beyond that of a singular plant community map. A total of 546,150 hectares of native vegetation in 100 native plant communities was mapped across the study area (Coolamon, Cootamundra, Junee, Lockhart, Narrandera, Tarcutta, Urana, Wagga Wagga and Yanco 1:100,000 mapsheets and Ariah Park, Wallaroobie Range and Yoogali 1:50,000 mapsheets). Exotic pine plantations and native species plantings were also mapped. Remnants of greater than one hectare were captured through on-screen GIS digitising at scales of approximately 1:4,000. The plant community type mapping was independently assessed using random blind validation points as having a user accuracy of 87%. This level of accuracy demonstrates the applicability of the methodology for mapping open forests, woodlands and open woodlands of south-eastern Australia and probably other vegetation elsewhere. Such accurate mapping provides end users with confidence when using vegetation maps in environmental assessment and land use planning

TGFbeta induces apoptosis and EMT in primary mouse hepatocytes independently of p53, p21Cip1 or Rb status

Melville Trust for the Care and Cure of Cancer to SP and SS.Background: TGF beta has pleiotropic effects that range from regulation of proliferation and apoptosis to morphological changes and epithelial-mesenchymal transition (EMT). Some evidence suggests that these effects may be interconnected. We have recently reported that P53, P21(Cip1) and pRB, three critical regulators of the G1/S transition are variably involved in TGF beta-induced cell cycle arrest in hepatocytes. As these proteins are also involved in the regulation of apoptosis in many circumstances, we investigated their contribution to other relevant TGF beta-induced effects, namely apoptosis and EMT, and examined how the various processes were interrelated. Methods: Primary mouse hepatocytes deficient in p53, p21 and/or Rb, singly or in combination were treated with TGF beta for 24 to 96 hours. Apoptosis was quantified according to morphology and by immunostaining for cleavedcapsase 3. Epithelial and mesenchymal marker expression was studied using immunocytochemistry and real time PCR. Results: We found that TGF beta similarly induced morphological changes regardless of genotype and independently of proliferation index or sensitivity to inhibition of proliferation by TGF beta. Morphological changes were accompanied by decrease in E-cadherin and increased Snail expression but the mesenchymal markers (N-cadherin, SMA alpha and Vimentin) studied remained unchanged. TGF beta induced high levels of apoptosis in p53-/-, Rb-/-, p21(cip1)-/- and control hepatocytes although with slight differences in kinetics. This was unrelated to proliferation or changes in morphology and loss of cell-cell adhesion. However, hepatocytes deficient in both p53 and p21(cip1)were less sensitive to TGF beta-induced apoptosis. Conclusion: Although p53, p21(Cip1) and pRb are well known regulators of both proliferation and apoptosis in response to a multitude of stresses, we conclude that they are critical for TGF beta-driven inhibition of hepatocytes proliferation, but only slightly modulate TGF beta-induced apoptosis. This effect may depend on other parameters such as proliferation and the presence of other regulatory proteins as suggested by the consequences of p53, p21(Cip1) double deficiency. Similarly, p53, p21(Cip1) and pRB deficiency had no effect on the morphological changes and loss of cell adhesion which is thought to be critical for metastasis. This indicates that possible association of these genes with metastasis potential would be unlikely to involve TGF beta-induced EMT.Publisher PDFPeer reviewe

Inositol Hexakisphosphate-Induced Autoprocessing of Large Bacterial Protein Toxins

Large bacterial protein toxins autotranslocate functional effector domains to the eukaryotic cell cytosol, resulting in alterations to cellular functions that ultimately benefit the infecting pathogen. Among these toxins, the clostridial glucosylating toxins (CGTs) produced by Gram-positive bacteria and the multifunctional-autoprocessing RTX (MARTX) toxins of Gram-negative bacteria have distinct mechanisms for effector translocation, but a shared mechanism of post-translocation autoprocessing that releases these functional domains from the large holotoxins. These toxins carry an embedded cysteine protease domain (CPD) that is activated for autoprocessing by binding inositol hexakisphosphate (InsP6), a molecule found exclusively in eukaryotic cells. Thus, InsP6-induced autoprocessing represents a unique mechanism for toxin effector delivery specifically within the target cell. This review summarizes recent studies of the structural and molecular events for activation of autoprocessing for both CGT and MARTX toxins, demonstrating both similar and potentially distinct aspects of autoprocessing among the toxins that utilize this method of activation and effector delivery

Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFβ cell cycle arrest

<p>Abstract</p> <p>Background</p> <p>TGFβ is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFβ in disease. We asked how <it>Rb</it>-deficiency would affect responses to TGFβ-induced cell cycle arrest.</p> <p>Results</p> <p>Primary hepatocytes isolated from <it>Rb-floxed </it>mice were infected with an adenovirus expressing CRE-recombinase to delete the <it>Rb </it>gene. In control cells treatment with TGFβ prevented cells to enter S phase via decreased cMYC activity, activation of P16^INK4Aand P21^Cipand reduction of E2F activity. In <it>Rb</it>-null hepatocytes, cMYC activity decreased slightly but P16^INK4Awas not activated and the great majority of cells continued cycling. <it>Rb </it>is therefore central to TGFβ-induced cell cycle arrest in hepatocytes. However some <it>Rb</it>-null hepatocytes remained sensitive to TGFβ-induced cell cycle arrest. As these hepatocytes expressed very high levels of P21^Cip1and P53 we investigated whether these proteins regulate pRb-independent signaling to cell cycle arrest by evaluating the consequences of disruption of <it>p53 </it>and <it>p21</it>^{<it>Cip1</it>}. Hepatocytes deficient in <it>p53 or p21</it>^{<it>Cip1 </it>}showed diminished growth inhibition by TGFβ. Double deficiency had a similar impact showing that in cells containing functional pRb; P21^Cipand P53 work through the same pathway to regulate G1/S in response to TGFβ. In <it>Rb</it>-deficient cells however, <it>p53 </it>but not <it>p21</it>^{<it>Cip </it>}deficiency had an additive effect highlighting a pRb-independent-P53-dependent effector pathway of inhibition of E2F activity.</p> <p>Conclusion</p> <p>The present results show that otherwise genetically normal hepatocytes with disabled <it>p53</it>, <it>p21</it>^{<it>Cip1 </it>}or <it>Rb </it>genes respond less well to the antiproliferative effects of TGFβ. As the function of these critical cellular proteins can be impaired by common causes of chronic liver disease and HCC, including viral hepatitis B and C proteins, we suggest that disruption of pRb function, and to a lesser extend P21^Cip1and P53 in hepatocytes may represent an additional new mechanism of escape from TGFβ-growth-inhibition in the inflammatory milieu of chronic liver disease and contribute to cancer development.</p