Consumer spaces as political spaces: a critical review of social, environmental and psychogeographical research

The purpose of this review is to critique the social and environmental psychology literature on spaces and places with a focus on consumer culture and neoliberalism. By drawing on social theory and the Continental philosophical literature the review argues that an alternative approach to knowledge production is required. To this end recommendations are provided for what a psychogeographical approach in social and environmental psychology could look like. It argues that such work could be of benefit to academic and local communities by exposing the social costs and consequences associated with consumer culture and neoliberalism

What does authenticity and neolocalism mean to craft brewery visitors? Insights from the Midwest and the Great Plains

The global rise in craft beer produced by small and independent brewers has precipitated the development of craft beer tourism. Two concepts, neolocalism and authenticity, have emerged as critical for understanding the craft beer experience. However, established research on these topics, particularly from the consumer perspective, are still quite limited. To fulfill this gap, this study conducted 46 semi-structured in-depth interviews and observations in breweries located in the Midwest and Great Plains regions to explore the meaning of authenticity and neolocalism to craft brewery visitors. Analysis resulted in nine major themes, including 1) beer itself, 2) beer production, 3) brewery accessibility, 4) brewery design, 5) vibes of brewery, 6) brewery services, 7) brewery place identity, 8) community engagement, and 9) local ownership. These findings enhance our conceptual understanding of neolocalism and authenticity from the craft beer visitors\u27 perspective. Potential implications and an agenda for future research are discussed

Comparison of T-cell Receptor Diversity of people with Myalgic Encephalomyelitis versus controls

Objective: Myalgic Encephalomyelitis (ME; sometimes referred to as Chronic Fatigue Syndrome) is a chronic disease without laboratory test, detailed aetiological understanding or effective therapy. Its symptoms are diverse, but it is distinguished from other fatiguing illnesses by the experience of post-exertional malaise, the worsening of symptoms even after minor physical or mental exertion. Its frequent onset after infection suggests autoimmune involvement or that it arises from abnormal T-cell activation. Results: To test this hypothesis, we sequenced the genomic loci of and T-cell receptors (TCR) from 40 human blood samples from each of four groups: severely affected people with ME; mildly or moderately affected people with ME; people diagnosed with Multiple Sclerosis, as disease controls; and, healthy controls. Seeking to automatically classify these individuals’ samples by their TCR repertoires, we applied P-SVM, a machine learning method. However, despite working well on a simulated data set, this approach did not allow statistically significant partitioning of samples into the four subgroups. Our findings do not support the hypothesis that blood samples from people with ME frequently contain altered T-cell receptor diversity

Identification of caspase 3 motifs and critical aspartate residues in human Phospholipase D1b and Phopsholipase D2a

Stimulation of mammalian cells frequently initiates phospholipase D-catalysed hydrolysis of phosphatidylcholine in the plasma membrane to yield phosphatidic acid (PA) a novel lipid messenger. PA plays a regulatory role in important cellular processes such as secretion, cellular shape change and movement. A number of studies have highlighted that PLD-based signalling also plays a pro-mitogenic and pro-survival role in cells and therefore anti-apoptotic. We show that human PLD1b and PLD2a contain functional caspase-3 cleavage sites and identify the critical aspartate residues within PLD1b that affect its activation by phorbol esters and attenuate phosphatidylcholine hydrolysis during apoptosis

Violation of the 12/23 rule of genomic V(D)J recombination is common in lymphocytes

V(D)J genomic recombination joins single gene segments to encode an extensive repertoire of antigen receptor specificities in T and B lymphocytes. This process initiates with double-stranded breaks adjacent to conserved recombination signal sequences that contain either 12- or 23-nucleotide spacer regions. Only recombination between signal sequences with unequal spacers results in productive coding genes, a phenomenon known as the '12/23 rule.' Here we present two novel genomic tools that allow the capture and analysis of immune locus rearrangements from whole thymic and splenic tissues using second-generation sequencing. Further, we provide strong evidence that the 12/23 rule of genomic recombination is frequently violated under physiological conditions, resulting in unanticipated hybrid recombinations in ∼10% of Tcra excision circles. Hence, we demonstrate that strict adherence to the 12/23 rule is intrinsic neither to recombination signal sequences nor to the catalytic process of recombination and propose that nonclassical excision circles are liberated during the formation of antigen receptor diversity

The N–Terminal Tail of hERG Contains an Amphipathic α–Helix That Regulates Channel Deactivation

The cytoplasmic N–terminal domain of the human ether–a–go–go related gene (hERG) K+ channel is critical for the slow deactivation kinetics of the channel. However, the mechanism(s) by which the N–terminal domain regulates deactivation remains to be determined. Here we show that the solution NMR structure of the N–terminal 135 residues of hERG contains a previously described Per–Arnt–Sim (PAS) domain (residues 26–135) as well as an amphipathic α–helix (residues 13–23) and an initial unstructured segment (residues 2–9). Deletion of residues 2–25, only the unstructured segment (residues 2–9) or replacement of the α–helix with a flexible linker all result in enhanced rates of deactivation. Thus, both the initial flexible segment and the α–helix are required but neither is sufficient to confer slow deactivation kinetics. Alanine scanning mutagenesis identified R5 and G6 in the initial flexible segment as critical for slow deactivation. Alanine mutants in the helical region had less dramatic phenotypes. We propose that the PAS domain is bound close to the central core of the channel and that the N–terminal α–helix ensures that the flexible tail is correctly orientated for interaction with the activation gating machinery to stabilize the open state of the channel

Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells

February 17, 2011The conversion of lineage-committed cells to induced pluripotent stem cells (iPSCs) by reprogramming is accompanied by a global remodeling of the epigenome[superscript 1, 2, 3, 4, 5], resulting in altered patterns of gene expression[superscript 2, 6, 7, 8, 9]. Here we characterize the transcriptional reorganization of large intergenic non-coding RNAs (lincRNAs)[superscript 10, 11] that occurs upon derivation of human iPSCs and identify numerous lincRNAs whose expression is linked to pluripotency. Among these, we defined ten lincRNAs whose expression was elevated in iPSCs compared with embryonic stem cells, suggesting that their activation may promote the emergence of iPSCs. Supporting this, our results indicate that these lincRNAs are direct targets of key pluripotency transcription factors. Using loss-of-function and gain-of-function approaches, we found that one such lincRNA (lincRNA-RoR) modulates reprogramming, thus providing a first demonstration for critical functions of lincRNAs in the derivation of pluripotent stem cells