The Trouble with Tourism

The hegemonic view of tourism is as a global panacea for struggling peoples, environments and economies (Smith and Brent 2001). This article begins by arguing that increasing worldwide risks from human-induced climate change fundamentally alter the veracity of this prediction claim. As one of the world’s largest industries, tourism is also one of the largest emitters of carbon, primarily from air transport. Far from standing apart from our carbon-dependent economy, tourism is quite profoundly a creation of that economy and cannot be an antidote to the very stuff of which it is made. Further, to the extent that tourism functions as escape from the ills of petroleum-driven life, it detracts critical attention and investment from home places and communities. The article concludes with a proposition for an alternative futures forecast based on bioregional tourism, or locavism. Characteristics of a locavist approach include the de-growth of the high-carbon, distant travel model of tourism and replacement with a low-carbon model that emphasizes local destinations, short distances, lower-carbon transport modes, and capital investment (both financial and social) in local communities

Public Perceptions on the Ideal Balance between Natural Resource Protection and Use in the Western USA

Attitudes of Western residents of the USA toward natural resources have been changing due to changes in demographics and rapid population growth in the region. The objective of the study reported here was to determine how residents in 15 Western states view the balance between natural resource exploitation and protection. In general, natural resource protection was more important than resource use for people having the following demographic characteristics: (1) female, (2) younger than 60, (3) more formally educated, and (4) residing in communities larger than 25,000

Common ELF1 deletion in prostate cancer bolsters oncogenic ETS function, inhibits senescence and promotes docetaxel resistance

ETS family transcription factors play major roles in prostate tumorigenesis with some acting as oncogenes and others as tumor suppressors. ETS factors can compete for binding at some cis-regulatory sequences, but display specific binding at others. Therefore, changes in expression of ETS family members during tumorigenesis can have complex, multimodal effects. Here we show that ELF1 was the most commonly down-regulated ETS factor in primary prostate tumors, and expression decreased further in metastatic disease. Genome-wide mapping in cell lines indicated that ELF1 has two distinct tumor suppressive roles mediated by distinct cis-regulatory sequences. First, ELF1 inhibited cell migration and epithelial-mesenchymal transition by interfering with oncogenic ETS functions at ETS/AP-1 cis-regulatory motifs. Second, ELF1 uniquely targeted and activated genes that promote senescence. Furthermore, knockdown of ELF1 increased docetaxel resistance, indicating that the genomic deletions found in metastatic prostate tumors may promote therapeutic resistance through loss of both RB1 and ELF1

One-step generation of high-quality squeezed and EPR states in cavity QED

We show how to generate bilinear (quadratic) Hamiltonians in cavity quantum electrodynamics (QED) through the interaction of a single driven three-level atom with two (one) cavity modes. With this scheme it is possible to generate one-mode mesoscopic squeezed superpositions, two-mode entanglements, and two-mode squeezed vacuum states (such the original EPR state), without the need for Ramsey zones and external parametric amplification. The degree of squeezing achieved is up to 99% with currently feasible experimental parameters and the errors due to dissipative mechanisms become practically negligible

Quantum-limited force measurement with an optomechanical device

We study the detection of weak coherent forces by means of an optomechanical device formed by a highly reflecting isolated mirror shined by an intense and highly monochromatic laser field. Radiation pressure excites a vibrational mode of the mirror, inducing sidebands of the incident field, which are then measured by heterodyne detection. We determine the sensitivity of such a scheme and show that the use of an entangled input state of the two sideband modes improves the detection, even in the presence of damping and noise acting on the mechanical mode.Comment: 8 pages, 4 figure

Electrostatic repulsion causes anticooperative DNA binding between tumor suppressor ETS transcription factors and JUN-FOS at composite DNA sites

Many different transcription factors (TFs) regulate gene expression in a combinatorial fashion, often by binding in close proximity to each other on composite cis-regulatory DNA elements. Here, we investigated how ETS TFs bind with the AP1 TFs JUN-FOS at composite DNA-binding sites. DNA-binding ability with JUN-FOS correlated with the phenotype of ETS proteins in prostate cancer. We found that the oncogenic ETS-related gene (ERG) and ETS variant (ETV) 1/4/5 subfamilies co-occupy ETS-AP1 sites with JUN-FOS in vitro, whereas JUN-FOS robustly inhibited DNA binding by the tumor suppressors ETS homologous factor (EHF) and SAM pointed domain-containing ETS TF (SPDEF). EHF bound ETS-AP1 DNA with tighter affinity than ERG in the absence of JUN-FOS, possibly enabling EHF to compete with ERG and JUN-FOS for binding to ETS-AP1 sites. Genome-wide mapping of EHF- and ERG-binding sites in prostate epithelial cells revealed that EHF is preferentially excluded from closely spaced ETS-AP1 DNA sequences. Structural modeling and mutational analyses indicated that adjacent positively charged surfaces from EHF and JUN-FOS use electrostatic repulsion to disfavor simultaneous DNA binding. Conservation of positive residues on the JUN-FOS interface identified E74-like ETS TF 1 (ELF1) as an additional ETS TF exhibiting anticooperative DNA binding with JUN-FOS, and we found that ELF1 is frequently down-regulated in prostate cancer. In summary, divergent electrostatic features of ETS TFs at their JUN-FOS interface enable distinct binding events at ETS-AP1 DNA sites, which may drive specific targeting of ETS TFs to facilitate distinct transcriptional programs

Ras/ERK and PI3K/AKT signaling differentially regulate oncogenic ERG mediated transcription in prostate cells

The TMPRSS2/ERG gene rearrangement occurs in 50% of prostate tumors and results in expression of the transcription factor ERG, which is normally silent in prostate cells. ERG expression promotes prostate tumor formation and luminal epithelial cell fates when combined with PI3K/AKT pathway activation, however the mechanism of synergy is not known. In contrast to luminal fates, expression of ERG alone in immortalized normal prostate epithelial cells promotes cell migration and epithelial to mesenchymal transition (EMT). Migration requires ERG serine 96 phosphorylation via endogenous Ras/ERK signaling. We found that a phosphomimetic mutant, S96E ERG, drove tumor formation and clonogenic survival without activated AKT. S96 was only phosphorylated on nuclear ERG, and differential recruitment of ERK to a subset of ERG-bound chromatin associated with ERG-activated, but not ERG-repressed genes. S96E did not alter ERG genomic binding, but caused a loss of ERG-mediated repression, EZH2 binding and H3K27 methylation. In contrast, AKT activation altered the ERG cistrome and promoted expression of luminal cell fate genes. These data suggest that, depending on AKT status, ERG can promote either luminal or EMT transcription programs, but ERG can promote tumorigenesis independent of these cell fates and tumorigenesis requires only the transcriptional activation function

ELK1 Uses Different DNA Binding Modes to Regulate Functionally Distinct Classes of Target Genes

Eukaryotic transcription factors are grouped into families and, due to their similar DNA binding domains, often have the potential to bind to the same genomic regions. This can lead to redundancy at the level of DNA binding, and mechanisms are required to generate specific functional outcomes that enable distinct gene expression programmes to be controlled by a particular transcription factor. Here we used ChIP–seq to uncover two distinct binding modes for the ETS transcription factor ELK1. In one mode, other ETS transcription factors can bind regulatory regions in a redundant fashion; in the second, ELK1 binds in a unique fashion to another set of genomic targets. Each binding mode is associated with different binding site features and also distinct regulatory outcomes. Furthermore, the type of binding mode also determines the control of functionally distinct subclasses of genes and hence the phenotypic response elicited. This is demonstrated for the unique binding mode where a novel role for ELK1 in controlling cell migration is revealed. We have therefore uncovered an unexpected link between the type of binding mode employed by a transcription factor, the subsequent gene regulatory mechanisms used, and the functional categories of target genes controlled

Squeezing of a coupled state of two spinors

The notion of spin squeezing involves reduction in the uncertainty of a component of the spin vector below a certain limit. This aspect has been studied earlier for pure and mixed states of definite spin. In this paper, this study has been extended to coupled spin states which do not possess sharp spin value. A general squeezing criterion has been obtained by requiring that a direct product state for two spinors is not squeezed. The squeezing aspect of entangled states is studied in relation to their spin- spin correlations.Comment: Typeset in LaTeX 2e using the style iopart, packages iopams,times,amssymb,graphicx; 17 pages, 5 eps figure file