What is generated through rupture?

Our commentary explores the contested possibilities of rupture, disaster, and emergency, and reflects on growing fears around political extremism. Rupture as theorised by Mahanty et al. captures the generative potential that arises through the conditions of the Anthropocene. We emphasise the political ambiguity of these processes and their potential to spur progressive possibility as well as political change that leans towards oppression and violence. We discuss how rupture can be purposefully catalysed or co-opted as a political tool by actors with starkly different aims, underscoring the importance of understanding the types of ruptures being generated and for whom these processes of change serve

Emergent spaces of emergency claims: Possibilities and contestation in a national climate emergency declaration

Climate emergency declarations have become a prominent mechanism within the environmental movement to emphasise the urgency of the climate crisis, with this activism prompting numerous declarations from governments. Embedded in these declarations are claims of emergency, which hold representations of how different actors make sense of the present political moment and imagine trajectories of change. We analyse the contested meanings of public emergency claims made by activists and the state in Aotearoa New Zealand’s national climate emergency declaration. Identifying three framings of emergency as an objective truth, an activating property, and a responsibility, our analysis suggests emergency declarations hold ambiguous potential for more radical action on climate change. While opening political space on what emergency means, we argue emergency claims hold risks of depoliticising climate politics and re-embedding the neoliberal status quo. Emergency claims also contain tensions in imaginaries of transformation, suggesting the importance of contestation within climate emergency declarations

Hydrocarbon Biogeochemical Setting of the Baffin Island Oil Spill Experimental Sites. II. Water

A baseline for petroleum residues in the waters of the Cape Hatt region of Baffin Island in arctic Canada was obtained in anticipation of controlled oil releases of the Baffin Island Oil Spill (BIOS) Project. Total aliphatic and aromatic residues reflecting multiple sources were found to be in the low to sub micro g/l concentrations range. Alkylated naphthalenes, phenanthrenes and dibenzothiophenes were present in the sub ng/l concentrations range. The hydrocarbon baseline for the waters of the BIOS study area was found to be as low as might be found anywhere on earth and therefore ideally suited to the BIOS study.Key words: BIOS, arctic marine Canada, hydrocarbon baseline, waterMots clés: BIOS, Arctique marin canadien, niveau de référence d’hydrocarbures, ea

Hydrocarbon Biogeochemical Setting of the Baffin Island Oil Spill Experimental Sites. I. Sediments

A baseline for petroleum residues in the sediments of the Cape Hatt Island in arctic Canada was obtained in anticipation of controlled oil releases of the Baffin Island Oil Spill (BIOS) Project. In subtidal sediments, the existing background of petroleum residues has an upper limit in the low to sub micro g/g concentration range. Petroleum was one of a variety of sources identified, including plant paraffin waxes and combustion products. Beach sediment hydrocarbons were quantitatively and qualitatively similar to those of subtidal sediments. The hydrocarbon baseline in sediments of the BIOS study area was found to be as low as might be found anywhere on earth and therefore ideally suited to the BIOS study.Key words: BIOS, arctic marine Canada, hydrocarbon baseline, sedimentsMots clés: BIOS, Arctique marin canadien, niveau de référence d'hydrocarbures, sédiment

Molecular cloning, expression analysis and assignment of the porcine tumor necrosis factor superfamily member 10 gene (TNFSF10) to SSC13q34 -> q36 by fluorescence in situ hybridization and radiation hybrid mapping

We have cloned the complete coding region of the porcine TNFSF10 gene. The porcine TNFSF10 cDNA has an ORF of 870 nucleotides and shares 85 % identity with human TNFSF10, and 75% and 72% identity with rat and mouse Tnfsf10 coding sequences, respectively. The deduced porcine TNFSF10 protein consists of 289 amino acids with the calculated molecular mass of 33.5 kDa and a predicted pI of 8.15. The amino acid sequence similarities correspond to 86, 72 and 70% when compared with human, rat and mouse sequences, respectively. Nor-them blot analysis detected TNFSF10-specific transcripts (similar to 1.7 kb) in various organs of a 10-week-old pig, suggesting ubiquitous expression. Real-time RT-PCR studies of various organs from fetal (days 73 and 98) and postnatal stages (two weeks, eight months) demonstrated developmental and tissue-specific regulation of TNFSF10 mRNA abundance. The chromosomal location of the porcine TNFSF10 gene was determined by FISH of a specific BAC clone to metaphase chromosomes. This TNFSF10 BAC clone has been assigned to SSC13q34 -> q36. Additionally, the localization of the TNFSF10 gene was verified by RH mapping on the porcine IMpRH panel. Copyright (c) 2005S. KargerAG, Basel

Hydrocarbon Biogeochemical Setting of the Baffin Island Oil Spill Experimental Sites. III. Biota

A baseline for petroleum residues in the Cape Hatt region of Baffin Island in arctic Canada was obtained in anticipation of controlled oil releases of the Baffin Island Oil Spill (BIOS) Project. Tissue hydrocarbons in a variety of arctic marine species were dominated by biogenic hydrocarbons. UV/F analysis of tissues indicated an upper limit of petroleum residues in the low to sub micro g/g concentration range. PAHs were detected in samples in the low ng/g concentration range and revealed a distribution of the combustion type. The hydrocarbon baseline in the BIOS study area was found to be as low as might be found anywhere on earth and therefore ideally suited to the BIOS study.Key words: BIOS, arctic marine Canada, hydrocarbon baseline, organismsMots clés: BIOS, Arctique marin canadien, niveau de référence d’hydrocarbures, organisme

Exploring the cultural dimensions of environmental victimization

It has become increasingly clear in recent years that our understanding of ‘victimisation’ is informed by a whole range of societal and political factors which extend well beyond whatever particular form of words appears in any given directive, code or legislative instrument concerning crime, crime victims or criminal justice systems. In this paper, I will seek for the first time to apply recent developments in our understanding of so-called 'cultural victimology' to the issue of environmental harm and its impact on human and non-human animals. McCGarry and Waklate (2015) characterise cultural victimology as broadly comprising of two key aspects. These are the wider sharing and reflection of individual and collective victimisation experiences on the one hand and, on the other, the mapping of those experiences through the criminal justice process. In this discussion I will examine how environmental victimisation is viewed by and presented to society at large and will argue that such representations often fail, as a form of testimony, to adequately convey the traumas involved. Nor is this achieved through the application of present models of criminal, civil or administrative justice regimes in many jurisdictions. This lack of cultural acknowledgement of the harms vested on environmental victims, it is argued, afford us a clearer understand of the continued reticence amongst lawmakers, politicians and legal practitioners to adequately address the impacts of such victimisation through effective justice or regulatory mechanisms. This is unfortunate given that the often collective nature of environmental victimisation makes this particularly suited to a more cultural analysis and understanding. It is argued that various forms of environmental mediation processes might hold the key to this cultural reticence to accept environmental harm as a 'real' and pressing problem as compared to other criminal and civil justice concerns

Implication of 4E-BP1 protein dephosphorylation and accumulation in pancreatic cancer cell death induced by combined gemcitabine and TRAIL

Pancreatic cancer cells show varying sensitivity to the anticancer effects of gemcitabine. However, as a chemotherapeutic agent, gemcitabine can cause intolerably high levels of toxicity and patients often develop resistance to the beneficial effects of this drug. Combination studies show that use of gemcitabine with the pro-apoptotic cytokine TRAIL can enhance the inhibition of survival and induction of apoptosis of pancreatic cancer cells. Additionally, following combination treatment there is a dramatic increase in the level of the hypophosphorylated form of the tumour suppressor protein 4E-BP1. This is associated with inhibition of mTOR activity, resulting from caspase-mediated cleavage of the Raptor and Rictor components of mTOR. Use of the pan-caspase inhibitor Z-VAD-FMK indicates that the increase in level of 4E-BP1 is also caspase-mediated. ShRNA-silencing of 4E-BP1 expression renders cells more resistant to cell death induced by the combination treatment. Since the levels of 4E-BP1 are relatively low in untreated pancreatic cancer cells these results suggest that combined therapy with gemcitabine and TRAIL could improve the responsiveness of tumours to treatment by elevating the expression of 4E-BP1

Cyclophosphamide Chemotherapy Sensitizes Tumor Cells to TRAIL-Dependent CD8 T Cell-Mediated Immune Attack Resulting in Suppression of Tumor Growth

Background: Anti-cancer chemotherapy can be simultaneously lymphodepleting and immunostimulatory. Pre-clinical models clearly demonstrate that chemotherapy can synergize with immunotherapy, raising the question how the immune system can be mobilized to generate anti-tumor immune responses in the context of chemotherapy. Methods and Findings: We used a mouse model of malignant mesothelioma, AB1-HA, to investigate T cell-dependent tumor resolution after chemotherapy. Established AB1-HA tumors were cured by a single dose of cyclophosphamide in a CD8 T cell- and NK cell-dependent manner. This treatment was associated with an IFN-α/β response and a profound negative impact on the anti-tumor and total CD8 T cell responses. Despite this negative effect, CD8 T cells were essential for curative responses. The important effector molecules used by the anti-tumor immune response included IFN-γ and TRAIL. The importance of TRAIL was supported by experiments in nude mice where the lack of functional T cells could be compensated by agonistic anti-TRAIL-receptor (DR5) antibodies. Conclusion: The data support a model in which chemotherapy sensitizes tumor cells for T cell-, and possibly NK cell-, mediated apoptosis. A key role of tumor cell sensitization to immune attack is supported by the role of TRAIL in tumor resolution and explains the paradox of successful CD8 T cell-dependent anti-tumor responses in the absence of CD8 T cell expansion

The functional significance of microRNA-145 in prostate cancer

BackgroundMicroRNAs (miRNAs) are small noncoding RNAs that have important roles in numerous cellular processes. Recent studies have shown aberrant expression of miRNAs in prostate cancer tissues and cell lines. On the basis of miRNA microarray data, we found that miR-145 is significantly downregulated in prostate cancer.Methods and resultsWe investigated the expression and functional significance of miR-145 in prostate cancer. The expression of miR-145 was low in all the prostate cell lines tested (PC3, LNCaP and DU145) compared with the normal cell line, PWR-1E, and in cancerous regions of human prostate tissue when compared with the matched adjacent normal. Overexpression of miR-145 in PC3-transfected cells resulted in increased apoptosis and an increase in cells in the G2/M phase, as detected by flow cytometry. Investigation of the mechanisms of inactivation of miR-145 through epigenetic pathways revealed significant DNA methylation of the miR-145 promoter region in prostate cancer cell lines. Microarray analyses of miR-145-overexpressing PC3 cells showed upregulation of the pro-apoptotic gene TNFSF10, which was confirmed by real-time PCR and western analysis.ConclusionOne of the genes significantly upregulated by miR-145 overexpression is the proapoptotic gene TNFSF10. Therefore, modulation of miR-145 may be an important therapeutic approach for the management of prostate cancer