Talking ‘bout poor folks (thinking ‘bout my folks): Perspectives on comparative poverty in working class households

This paper explores concepts and narratives of comparative poverty articulated by residents of six working class neighbourhoods in Britain and examines how individuals’ assessments of self were influenced by comparisons to other social groups. The paper presents empirical findings to suggest the need for more nuanced sociological and policy understandings of working class experience and alternative explanations for quiescence with inequality. Our findings suggest disconnections between research emphasising relative deprivation and stigmatisation, a drive to evaluate economic status and the centrality of a comparative relational framework for perceptions of poverty; and the actual lens’ through which many working class individuals conceptualise their circumstances. The denial of a social comparative paradigm was generated by circumstances being doxic (or taken for granted), the rejection of a ‘poverty’ label, the importance of self-trajectories and the ambivalent and nuanced relationships between material wealth, happiness and moral worth. However, a limited comparative gaze upon more affluent groups was contrasted with strong narratives of respectability and legitimacy juxtaposed with those groups deemed not to adhere to these working class values. The paper concludes by discussing the implications of these findings for housing policy

Gamers or victims of the system? Welfare reform, cynical manipulation and vulnerability

New mechanisms of conditionality enacted through current reforms of the UK welfare system are framed within contested narratives about the characteristics, rationalities and conduct of welfare users. In the problem figuration of welfare reform the orientations and conduct of welfare recipients have been conceptualised and depicted across a spectrum ranging from cynical manipulators gaming the system and subverting the original ethos of the welfare state to vulnerable individuals experiencing compounded disadvantage. This paper aims to strengthen the conceptualisation of cynical manipulation and vulnerability and to empirically investigate how narratives of these ideas are deployed by key stakeholders in the welfare system and the extent to which manipulation or vulnerability are present in the orientations and conduct of individuals in receipt of welfare support

Pharmacological characterization of the αvβ6 integrin binding and internalization kinetics of the foot-and-mouth disease virus derived peptide A20FMDV2

A20FMDV2 is a peptide derived from the foot-and-mouth disease virus with a high affinity and selectivity for the alphav beta-6 (αvβ6) arginyl-glycinyl-aspartic acid (RGD)-binding integrin. It has been shown to be an informative tool ligand in pre-clinical imaging studies for selective labelling of the αvβ6 integrin in a number of disease models. In a radioligand- binding assay using a radiolabelled form of the peptide ([3H]A20FMDV2), its high affinity (KD:0.22nmol/l) and selectivity (at least 85-fold) for αvβ6 over the other members of the RGD integrin family was confirmed. [3H]A20FMDV2 αvβ6 binding could be fully reversed only in the presence of EDTA, whereas a partial reversal was observed in the presence of excess concentrations of an RGD-mimetic small molecule (SC-68448) or unlabelled A20FMDV2. Using flow cytometry on bronchial epithelial cells, the ligand-induced internalization of αvβ6 by A20FMDV2 and LAP1 was shown to be fast (t1/2:1.5and 3.1 min, respectively), concentration-dependent (EC50:values 1.1 and 3.6nmol/l, respectively) and was followed by a moderately slow return of integrin to the surface. The results of the radioligand-binding studies suggest that the binding of A20FMDV2 to the RGD-binding site on αvβ6 is required to maintain its engagement with the hypothesised A20FMDV2 synergy site on the integrin. In addition, there is evidence from flow cytometric studies that the RGD-ligand engagement of αvβ6 post-internalization plays a role in delaying recycling of the integrin to the cell surface. This mechanism may act as a homeostatic control of membrane αvβ6 following RGD ligand engagement

Hybrid Decay: A Transgenerational Epigenetic Decline in Vigor and Viability Triggered in Backcross Populations of Teosinte with Maize.

In the course of generating populations of maize with teosinte chromosomal introgressions, an unusual sickly plant phenotype was noted in individuals from crosses with two teosinte accessions collected near Valle de Bravo, Mexico. The plants of these Bravo teosinte accessions appear phenotypically normal themselves and the F1 plants appear similar to typical maize × teosinte F1s. However, upon backcrossing to maize, the BC1 and subsequent generations display a number of detrimental characteristics including shorter stature, reduced seed set, and abnormal floral structures. This phenomenon is observed in all BC individuals and there is no chromosomal segment linked to the sickly plant phenotype in advanced backcross generations. Once the sickly phenotype appears in a lineage, normal plants are never again recovered by continued backcrossing to the normal maize parent. Whole-genome shotgun sequencing reveals a small number of genomic sequences, some with homology to transposable elements, that have increased in copy number in the backcross populations. Transcriptome analysis of seedlings, which do not have striking phenotypic abnormalities, identified segments of 18 maize genes that exhibit increased expression in sickly plants. A de novo assembly of transcripts present in plants exhibiting the sickly phenotype identified a set of 59 upregulated novel transcripts. These transcripts include some examples with sequence similarity to transposable elements and other sequences present in the recurrent maize parent (W22) genome as well as novel sequences not present in the W22 genome. Genome-wide profiles of gene expression, DNA methylation, and small RNAs are similar between sickly plants and normal controls, although a few upregulated transcripts and transposable elements are associated with altered small RNA or methylation profiles. This study documents hybrid incompatibility and genome instability triggered by the backcrossing of Bravo teosinte with maize. We name this phenomenon "hybrid decay" and present ideas on the mechanism that may underlie it

Cumulative mutagenesis of the basic residues in the 201-218 region of insulin-like growth factor (IGF)-binding protein-5 results in progressive loss of both IGF-I binding and inhibition of IGF-I biological action

We have reported previously that mutation of two conserved nonbasic amino acids (G203 and Q209) within the highly basic 201–218 region in the C-terminal domain of IGF-binding protein-5 (IGFBP-5) decreases binding to IGFs. This study reveals that cumulative mutagenesis of the 10 basic residues in this region, to create the C-Term series of mutants, ultimately results in a 15-fold decrease in the affinity for IGF-I and a major loss in heparin binding. We examined the ability of mutants to inhibit IGF-mediated survival of MCF-7 cells and were able to demonstrate that this depended not only upon the affinity for IGF-I, but also the kinetics of this interaction, because IGFBP-5 mutants with similar affinity constants (KD) values, but with different association (Ka) and dissociation (Kd) rate values, had markedly different inhibitory properties. In contrast, the affinity for IGF-I provided no predictive value in terms of the ability of these mutants to enhance IGF action when bound to the substratum. Instead, these C-Term mutants appeared to enhance the actions of IGF-I by a combination of increased dissociation of IGF-IGFBP complexes from the substratum, together with dissociation of IGF-I from IGFBP-5 bound to the substratum. These effects of the IGFBPs were dependent upon binding to IGF-I, because a non-IGF binding mutant (N-Term) was unable to inhibit or enhance the actions of IGF-I. These results emphasize the importance of the kinetics of association/dissociation in determining the enhancing or inhibiting effects of IGFBP-5 and demonstrate the ability to generate an IGFBP-5 mutant with exclusively IGF-enhancing activity

The Lantern Vol. 31, No. 2, May 1964

• The High, Forbidding Wall • Sonnet One • Sceptic • The Witch, the Prince, and the Princess • Portrait in Gold and Black • The Music of the Drum • Sweat It, Jack • Cold Blue and the Moon • Another Carpenter: Circa 1963 • At a Conference of Colonial Historians • Pineland Places • Diasia to Death • Hey!... • The Hour • I\u27ll Not Returnhttps://digitalcommons.ursinus.edu/lantern/1086/thumbnail.jp

Rational Fictions and Imaginary Systems: Cynical Ideology and the Problem Figuration and Practise of Public Housing

This paper aims to show how Van Wel's theory of problem figuration, Carlen's concept of imaginary systems and Zizek's notion of cynical ideology may advance our theoretical and empirical understanding of the contemporary construction of housing policy narratives and embedded localised housing practise. Applying this theoretical framework to a case study of responses to homelessness in Scotland and further illustrative examples from the UK and the USA, the paper examines how housing practise is constituted through different imaginaries of housing systems. These are based on fictional as well as rational elements, located within a form of cynical ideology whereby actors act ‘as if’ the realities of the present housing crisis are distanced from the imagined intended functioning of housing systems. This masks alternative social realities and denies an explicitly articulated politics of housing which would reveal new processes of capitalism, generational and class realignments and a reframing of the role of government itself

Clinically Approved Heterocyclics Act on a Mitochondrial Target and Reduce Stroke-induced Pathology

Substantial evidence indicates that mitochondria are a major checkpoint in several pathways leading to neuronal cell death, but discerning critical propagation stages from downstream consequences has been difficult. The mitochondrial permeability transition (mPT) may be critical in stroke-related injury. To address this hypothesis, identify potential therapeutics, and screen for new uses for established drugs with known toxicity, 1,040 FDA-approved drugs and other bioactive compounds were tested as potential mPT inhibitors. We report the identification of 28 structurally related drugs, including tricyclic antidepressants and antipsychotics, capable of delaying the mPT. Clinically achievable doses of one drug in this general structural class that inhibits mPT, promethazine, were protective in both in vitro and mouse models of stroke. Specifically, promethazine protected primary neuronal cultures subjected to oxygen-glucose deprivation and reduced infarct size and neurological impairment in mice subjected to middle cerebral artery occlusion/reperfusion. These results, in conjunction with new insights provided to older studies, (a) suggest a class of safe, tolerable drugs for stroke and neurodegeneration; (b) provide new tools for understanding mitochondrial roles in neuronal cell death; (c) demonstrate the clinical/experimental value of screening collections of bioactive compounds enriched in clinically available agents; and (d) provide discovery-based evidence that mPT is an essential, causative event in stroke-related injury