Securing conservation Lebensraum? The geo-, bio-, and ontopolitics of global conservation futures

The geographical concept of Lebensraum ("living space") was coined most significantly by the German scholar Friedrich Ratzel towards the end of the nineteenth century. Through the lens of Lebensraum, Ratzel reformulated Darwin's conception of evolution as a "struggle for life" into a "struggle for space", highlighting how nonhuman species - as well as biologically conceived human 'races', nations, states, and empires - grew organically in space and colonized it. Although the concept attained considerable influence in the first half of the twentieth century, after World War II it largely fell into disrepute due to its various imperialist, colonialist, and fascist associations. Yet in some ways, contemporary academic debates concerning land and resource governance continue to implicitly or partially evoke the substance of certain Lebensraum conceptualizations. This is particularly so with respect to debates about global biodiversity conservation. Revisiting both Ratzelian and other fin-de-siecle theorizations of Lebensraum, we argue that contemporary efforts to reformulate conservation governance at the planetary scale risk amounting to a form of what we term "conservation Lebensraum", or a globally-significant "struggle for conservation space". Analysing the implications of conservation Lebensraum through a tripartite conceptual framework at the intersection of conservation biopolitics, geopolitics, and ontopolitics, we highlight how global biodiversity conservation initiatives seek to respond to multiple socio-ecological crises in the so-called Anthropocene. We end with a brief discussion of more socio-ecologically just alternatives to conservation Lebensraum, thereby contributing to critical conversations about the political ecology of emergent conservation futures

Law School Based Public Interest Advocacy: An Australian Story

This article presents a case for law schools to undertake public interest advocacy. It argues that incorporating public interest advocacy into curricula and research enhances clinical legal education and enables law schools to make a distinctive and valuable contribution to justice and law reform. The article outlines an integrated model for law school based public interest advocacy based on the experience of one of Australia’s newest law schools at Newcastle in the Hunter region of New South Wales. The article then describes a recent public interest case undertaken by academics, clinicians and students at Newcastle law school, explaining their participation in the case and exploring the contributions made by the case to legal education, the correction of injustice and reform of the law.The case, one of Australia’s most controversial deaths in custody, concerned the fatal shooting on Bondi Beach in Sydney in June 1997 of French photographer Roni Levi. The article examines the shooting, its investigation by police, a coroner and an independent commission of inquiry. It analyses the flaws in these legal investigations, considers their justice implications, and outlines the legal and policing reforms achieved through the case.The article concludes with the suggestion that changes in law school culture as well as curriculum are needed to ensure that law schools embrace public interest advocacy and other forms of clinical legal education for the future benefit of the law and its students

National environmental policy during the Clinton years

We review major developments in national environmental policy during the Clinton Administration, defining environmental policy to include not only the statutes, regulations, and policies associated with reducing pollution, but also major issues of public lands management and species preservation. We adopt economic criteria for policy assessment — principally efficiency, cost-effectiveness, and distributional equity. While the paper is primarily descriptive, we highlight a set of themes that emerge in the economics of national environmental policy over the past decade

Exposure to a Nonionic Surfactant Induces a Response Akin to Heat-Shock Apoptosis in Intestinal Epithelial Cells: Implications for Excipients Safety

© 2019 American Chemical Society. Amphipathic, nonionic, surfactants are widely used in pharmaceutical, food, and agricultural industry to enhance product features; as pharmaceutical excipients, they are also aimed at increasing cell membrane permeability and consequently improving oral drugs absorption. Here, we report on the concentration- and time-dependent succession of events occurring throughout and subsequent exposure of Caco-2 epithelium to a "typical" nonionic surfactant (Kolliphor HS15) to provide a molecular explanation for nonionic surfactant cytotoxicity. The study shows that the conditions of surfactant exposure, which increase plasma membrane fluidity and permeability, produced rapid (within 5 min) redox and mitochondrial effects. Apoptosis was triggered early during exposure (within 10 min) and relied upon an initial mitochondrial membrane hyperpolarization (5-10 min) as a crucial step, leading to its subsequent depolarization and caspase-3/7 activation (60 min). The apoptotic pathway appears to be triggered prior to substantial surfactant-induced membrane damage (observed ≥60 min). We hence propose that the cellular response to the model nonionic surfactant is triggered via surfactant-induced increase in plasma membrane fluidity, a phenomenon akin to the stress response to membrane fluidization induced by heat shock, and consequent apoptosis. Therefore, the fluidization effect that confers surfactants the ability to enhance drug permeability may also be intrinsically linked to the propagation of their cytotoxicity. The reported observations have important implications for the safety of a multitude of nonionic surfactants used in drug delivery formulations and to other permeability enhancing compounds with similar plasma membrane fluidizing mechanisms

Muffled price signals: Household water demand under increasing-block prices

In many areas of the world, including large parts of the United States, scarce water supplies are a serious resource and environmental concern. The possibility exists that water is being used at rates that exceed what would be dictated by efficiency criteria, particularly when externalities are taken into account. Because of this, much attention has been given by policy makers and others to the use of various techniques of demand management, including requirements for the adoption of specific technologies and restrictions on particular uses. A natural question for economists to ask is whether price would be a more effective instrument to facilitate efficient management of water resources. As a first step in such an investigation, this paper draws upon a newly available set of detailed data to estimate econometrically the demand function for household use of urban water supplies. Because of the diverse multiple-block pricing structures that abound, estimation of this relationship poses some challenging and interesting problems

An investigation into mechanisms of non-ionic surfactant effect on epithelial cells

Amphipathic, non-ionic surfactants are widely used in pharmaceutical and food industries to enhance product features; as pharmaceutical excipients they achieve increased cell membrane permeability and consequently can improve the oral absorption of drugs across the intestinal epithelial barrier. The use of non-ionic surfactants has grown rapidly, and is predicted to increase, however, the mechanism(s) surrounding the induction of surfactant toxicity is not well established and, consequently, the potential risks of surfactant exposure are not well understood. This work studies the concentration- and time-dependent succession of events that occur during and following exposure of an intestinal epithelial cell model to a ‘typical’ non-ionic surfactant – Solutol HS15. The resulted gathered demonstrate that prior to a significant increase in membrane permeability to a model drug (FITC-dextran 4kDa), non-ionic surfactant, at concentrations above its critical micellar concentration (CMC), produced almost immediate redox and mitochondrial effects manifested as an increased NADH pool, increased ROS levels, and hyperpolarisation of the mitochondrial membrane potential. Apoptosis was triggered early in this initial phase, and relied on mitochondrial hyperpolarisation as a crucial step leading to subsequent depolarisation and caspase-3/7 activation. Inhibition of mitochondrial hyperpolarisation prolonged cell survival, delayed the onset of metabolic reduction by the mitochondrial, and inhibited caspase activation. The apoptotic cell death pathway appears to be triggered prior to the emergence of substantial membrane damage by the surfactant: loss of plasma membrane integrity, nuclear membrane permeabilisation, and perturbations in calcium homeostasis - indicators of a necrotic process. It is proposed that the rapid cellular response is triggered via rapid surfactant-induced increases in plasma membrane fluidity; a phenomenon akin to the membrane-regulated stress response following membrane fluidisation by heat shock, and consequently cell death events. Furthermore, work performed on differentiated Caco-2 monolayers, alongside culture models replicating the basement membrane and paracrine signalling, demonstrate surfactant toxicity is reduced. Toxicity in vivo is therefore predicted to be less than measured on the standard model

A Novel Pool of Microparticle Cholesterol Is Elevatedin Rheumatoid Arthritis but Not in Systemic Lupus Erythematosus Patients

Microparticles are sub-micron, membrane-bound particles released from virtually allcells and which are present in the circulation. In several autoimmune disorders their amountand composition in the circulation is altered. Microparticle surface protein expression has beenexplored as a differentiating tool in autoimmune disorders where the clinical pictures can overlap.Here, we examine the utility of a novel lipid-based marker—microparticle cholesterol, present in allmicroparticles regardless of cellular origin—to distinguish between rheumatoid arthritis (RA) andsystemic lupus erythematosus (SLE). We first isolated a series of microparticle containing lipoproteindeficient fractions from patient and control plasma. There were no significant differences in thesize, structure or protein content of microparticles isolated from each group. Compared to controls,both patient groups contained significantly greater amounts of platelet and endothelial cell-derivedmicroparticles. The cholesterol content of microparticle fractions isolated from RA patients wassignificantly greater than those from either SLE patients or healthy controls. Our data indicate thatcirculating non-lipoprotein microparticle cholesterol, which may account for 1–2% of measuredcholesterol in patient samples, may represent a novel differentiator of disease, which is independentof cellular origi