Challenging the field: Bourdieu and men's health

©2014 Macmillan Publishers Ltd. This article considers how understandings of health promotion with men may be assisted by engagement with Bourdieu's theoretical work. The article outlines leading concepts within Bourdieu's work on 'field', 'habitus' and 'capital'; considers subsequent critical debates among gender, feminist and sociological theorists around structure and agency; and links these to discussions within men's health. A particular focus concerns structural disruption of, and movement of social actors between, 'fields' such as family, work and leisure settings. The article examines, through Bourdieu's critical legacy, whether such disruption establishes conditions for transformative reflexivity among men in relation to previously held dispositions (habitus), including those inflected by masculinities, that affect men's health practices. Recent work within Bourdieu's heritage potentially facilitates a re-framing of understandings of men's health practices. The article specifically explores masculine ambivalence within accounts of reflexivity, identities and practice, and considers how social and symbolic (masculine) capital are in play. Implications of Bourdieu's leading concepts for theorising settings-focused approaches to men's health promotion are exemplified with reference to a men's health project in a football stadium leisure setting. The article considers the benefits and challenges of applying gendered critical insights drawing on Bourdieu's work to men's health promotion, and discusses emerging theoretical dilemmas

Detection of Oxidation Products of 5-Methyl-2′-Deoxycytidine in Arabidopsis DNA

Epigenetic regulations play important roles in plant development and adaptation to environmental stress. Recent studies from mammalian systems have demonstrated the involvement of ten-eleven translocation (Tet) family of dioxygenases in the generation of a series of oxidized derivatives of 5-methylcytosine (5-mC) in mammalian DNA. In addition, these oxidized 5-mC nucleobases have important roles in epigenetic remodeling and aberrant levels of 5-hydroxymethyl-29-deoxycytidine (5-HmdC) were found to be associated with different types of human cancers. However, there is a lack of evidence supporting the presence of these modified bases in plant DNA. Here we reported the use of a reversed-phase HPLC coupled with tandem mass spectrometry method and stable isotope-labeled standards for assessing the levels of the oxidized 5-mC nucleosides along with two other oxidatively induced DNA modifications in genomic DNA of Arabidopsis. These included 5- HmdC, 5-formyl-29-deoxycytidine (5-FodC), 5-carboxyl-29-deoxycytidine (5-CadC), 5-hydroxymethyl-29-deoxyuridine (5- HmdU), and the (59S) diastereomer of 8,59-cyclo-29-deoxyguanosine (S-cdG). We found that, in Arabidopsis DNA, the levels of 5-HmdC, 5-FodC, and 5-CadC are approximately 0.8 modifications per 106 nucleosides, with the frequency of 5-HmdC (per 5-mdC) being comparable to that of 5-HmdU (per thymidine). The relatively low levels of the 5-mdC oxidation products suggest that they arise likely from reactive oxygen species present in cells, which is in line with the lack of homologous Tetfamily dioxygenase enzymes in Arabidopsis

Zum Zusammenhang von Geschlechterungleichheiten in Bildung, Beruf und Karriere : ein Ausblick

Ziel der folgenden Ausführungen im abschliessenden Teil dieses Sammelbands zur Entwicklung und Genese von geschlechtsspezifischen Bildungsungleichheiten ist es, den Blick zu öffnen in Richtung Berufsleben. Wie sind die verbesserten Bildungsmöglichkeiten von Frauen zu interpretieren? Ist es in den letzten Jahrzehnten gelungen, eines der grundlegendsten gesellschaftlichen Ungleichheitsverhältnisse zu beseitigen? Oder beginnt sich dieses sogar zu verkehren in eine gesellschaftliche Benachteiligung der Männer? Wir gehen bei unseren Überlegungen von der These aus, dass ein Abbau von Benachteiligungen der Frauen im Bildungssystem für sich genommen noch wenig aussagekräftig ist, wenn wir uns mit der klassischen soziologischen Frage der Persistenz bzw. des Wandels von gesellschaftlichen Ungleichheiten befassen wollen. Erst wenn die ganze Verknüpfung von Bildung und gesellschaftlicher Ungleichheit in den Blick genommen wird und sich dabei zeigt, dass Frauen ihre Bildungsgewinne auch in entsprechende Chancen im Beschäftigungssystem umsetzen können, sind ihre verbesserten Bildungschancen ein Gewinn für die Individuen und ein Fortschritt für die Gesellschaft – und erst dann könnten mögliche Bildungsvorteile von Frauen, wie sie in den vorliegenden Aufsätzen z.T. diagnostiziert werden, gar als neue gesellschaftliche Benachteiligungen von Männern skandalisiert werden

Genetic Separation of BRCA1 Functions Reveal Mutation-Dependent Polθ Vulnerabilities

Homologous recombination (HR)-deficiency induces a dependency on DNA polymerase theta (Polθ/Polq)-mediated end joining, and Polθ inhibitors (Polθi) are in development for cancer therapy. BRCA1 and BRCA2 deficient cells are thought to be synthetic lethal with Polθ, but whether distinct HR gene mutations give rise to equivalent Polθ-dependence, and the events that drive lethality, are unclear. In this study, we utilized mouse models with separate Brca1 functional defects to mechanistically define Brca1-Polθ synthetic lethality. Surprisingly, homozygous Brca1 mutant, Polq−/− cells were viable, but grew slowly and had chromosomal instability. Brca1 mutant cells proficient in DNA end resection were significantly more dependent on Polθ for viability; here, treatment with Polθi elevated RPA foci, which persisted through mitosis. In an isogenic system, BRCA1 null cells were defective, but PALB2 and BRCA2 mutant cells exhibited active resection, and consequently stronger sensitivity to Polθi. Thus, DNA end resection is a critical determinant of Polθi sensitivity in HR-deficient cells, and should be considered when selecting patients for clinical studies

The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin.

Breast and ovarian cancer patients harboring BRCA1/2 germline mutations have clinically benefitted from therapy with PARP inhibitor (PARPi) or platinum compounds, but acquired resistance limits clinical impact. In this study, we investigated the impact of mutations on BRCA1 isoform expression and therapeutic response. Cancer cell lines and tumors harboring mutations in exon 11 of BRCA1 express a BRCA1-Δ11q splice variant lacking the majority of exon 11. The introduction of frameshift mutations to exon 11 resulted in nonsense-mediated mRNA decay of full-length, but not the BRCA1-Δ11q isoform. CRISPR/Cas9 gene editing as well as overexpression experiments revealed that the BRCA1-Δ11q protein was capable of promoting partial PARPi and cisplatin resistance relative to full-length BRCA1, both in vitro and in vivo Furthermore, spliceosome inhibitors reduced BRCA1-Δ11q levels and sensitized cells carrying exon 11 mutations to PARPi treatment. Taken together, our results provided evidence that cancer cells employ a strategy to remove deleterious germline BRCA1 mutations through alternative mRNA splicing, giving rise to isoforms that retain residual activity and contribute to therapeutic resistance. Cancer Res; 76(9); 2778-90. ©2016 AACR