238 research outputs found

    Language and gender in political debates in the House of Commons

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    This thesis investigates the linguistic practices of politicians in one of the oldest and most powerful of all British institutions: the House of Commons. After the general election of 1997 record numbers of women were elected to parliament. This rapid increase in women's representation led to much speculation in politics and the media about how new women MPs would adapt to and change British politics. At the same time it is clear that men and women MPs are not treated equally. Women are marginalised by sexist barracking within the chamber and portrayed negatively by the media.\ud Theoretical and methodological insights gained from language and gender research are used to explore whether this inequality extends to the differential access to and use of linguistic resources by women and men in the debating chamber. The central questions of the thesis are: what factors contribute to a participant being more or less powerful in this context, and how salient is gender to the construction of that power? Viewing the debating chamber as a 'Community of Practice' (Eckert and McConnell-Ginet 1992), and drawing upon the insights of MPs from interview data, I describe the interactional norms of the House of Commons as part of the ethnographic approach to this research. Using data from a 60-hour video corpus of House of Commons speech events I then undertake an analysis of floor apportionment in debates. I identify adversarial linguistic features in parliamentary question time sessions and examine their use by women and men. I also undertake an analysis of the functions and use of humour and irony in the debating chamber. Finally, a comparative study is undertaken with the Scottish Parliament. I describe the parliamentary procedures and historical development of the Scottish Parliament before analysing floor apportionment, the use of adversarial language, and humour and irony in this forum. \u

    Evolution of a Canada Basin ice-ocean boundary layer and mixed layer across a developing thermodynamically forced marginal ice zone

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    A comprehensive set of autonomous, ice-ocean measurements were collected across the Canada Basin to study the summer evolution of the ice-ocean boundary layer (IOBL) and ocean mixed layer (OML). Evaluation of local heat and freshwater balances and associated turbulent forcing reveals that melt ponds (MPs) strongly influence the summer IOBL-OML evolution. Areal expansion of MPs in mid-June start the upper ocean evolution resulting in significant increases to ocean absorbed radiative flux (19 W m−2 in this study). Buoyancy provided by MP drainage shoals and freshens the IOBL resulting in a 39 MJ m−2 increase in heat storage in just 19 days (52% of the summer total). Following MP drainage, a near-surface fresh layer deepens through shear-forced mixing to form the summer mixed layer (sML). In late summer, basal melt increases due to stronger turbulent mixing in the thin sML and the expansion of open water areas due in part to wind-forced divergence of the sea ice. Thermal heterogeneities in the marginal ice zone (MIZ) upper ocean led to large ocean-to-ice heat fluxes (100–200 W m−2) and enhanced basal ice melt (3–6 cm d−1), well away from the ice edge. Calculation of the upper ocean heat budget shows that local radiative heat input accounted for at least 89% of the observed latent heat losses and heat storage (partitioned 0.77/0.23). These results suggest that the extensive area of deteriorating sea ice observed away from the ice edge during the 2014 season, termed the “thermodynamically forced MIZ,” was driven primarily by local shortwave radiative forcing

    Distribution, organization and expression of genes concerned with anaerobic lactate utilization in human intestinal bacteria

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    Lactate accumulation in the human gut is linked to a range of deleterious health impacts. However, lactate is consumed and converted to the beneficial short-chain fatty acids butyrate and propionate by indigenous lactate-utilizing bacteria. To better understand the underlying genetic basis for lactate utilization, transcriptomic analyses were performed for two prominent lactate-utilizing species from the human gut, Anaerobutyricum soehngenii and Coprococcus catus , during growth on lactate, hexose sugar or hexose plus lactate. In A. soehngenii L2-7 six genes of the lactate utilization (lct) cluster, including NAD-independent d-lactate dehydrogenase (d-iLDH), were co-ordinately upregulated during growth on equimolar d- and l-lactate (dl-lactate). Upregulated genes included an acyl-CoA dehydrogenase related to butyryl-CoA dehydrogenase, which may play a role in transferring reducing equivalents between reduction of crotonyl-CoA and oxidation of lactate. Genes upregulated in C. catus GD/7 included a six-gene cluster (lap) encoding propionyl CoA-transferase, a putative lactoyl-CoA epimerase, lactoyl-CoA dehydratase and lactate permease, and two unlinked acyl-CoA dehydrogenase genes that are candidates for acryloyl-CoA reductase. A d-iLDH homologue in C. catus is encoded by a separate, partial lct, gene cluster, but not upregulated on lactate. While C. catus converts three mols of dl-lactate via the acrylate pathway to two mols propionate and one mol acetate, some of the acetate can be re-used with additional lactate to produce butyrate. A key regulatory difference is that while glucose partially repressed lct cluster expression in A. soehngenii , there was no repression of lactate-utilization genes by fructose in the non-glucose utilizer C. catus . This suggests that these species could occupy different ecological niches for lactate utilization in the gut, which may be important factors to consider when developing lactate-utilizing bacteria as novel candidate probiotics

    PRL-3, a Metastasis Associated Tyrosine Phosphatase, Is Involved in FLT3-ITD Signaling and Implicated in Anti-AML Therapy

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    Combination with other small molecule drugs represents a promising strategy to improve therapeutic efficacy of FLT3 inhibitors in the clinic. We demonstrated that combining ABT-869, a FLT3 inhibitor, with SAHA, a HDAC inhibitor, led to synergistic killing of the AML cells with FLT3 mutations and suppression of colony formation. We identified a core gene signature that is uniquely induced by the combination treatment in 2 different leukemia cell lines. Among these, we showed that downregulation of PTP4A3 (PRL-3) played a role in this synergism. PRL-3 is downstream of FLT3 signaling and ectopic expression of PRL-3 conferred therapeutic resistance through upregulation of STAT (signal transducers and activators of transcription) pathway activity and anti-apoptotic Mcl-1 protein. PRL-3 interacts with HDAC4 and SAHA downregulates PRL-3 via a proteasome dependent pathway. In addition, PRL-3 protein was identified in 47% of AML cases, but was absent in myeloid cells in normal bone marrows. Our results suggest such combination therapies may significantly improve the therapeutic efficacy of FLT3 inhibitors. PRL-3 plays a potential pathological role in AML and it might be a useful therapeutic target in AML, and warrant clinical investigation
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