24 research outputs found

    A critical analysis of post-legislative scrutiny in the UK Parliament

    Get PDF
    PhD ThesisPost-legislative scrutiny in the UK Parliament became a formal part of committee activity in 2008 and to date there have been no systematic studies either in the UK or elsewhere. The limited literature that does exist on post-legislative scrutiny is restricted mainly to parliamentary reports. As such this research helps to fill an important gap in the academic literature. The thesis contributes to the conceptual understanding of scrutiny, accountability and responsibility as well as how these concepts interact with and impact upon post-legislative scrutiny. The research follows a mixed methods approach, focusing upon the content analysis of postlegislative scrutiny reports with a particular focus upon the recommendations made and their acceptance by the government. These findings are supported by several case studies of post-legislative scrutiny inquiries. Drawing upon interviews with stakeholders, these case studies permit examination of the process of postlegislative scrutiny in much greater detail. The research finds that while post-legislative scrutiny is more extensive than it first appears, the majority of committees do not engage with it formally. There is also a selection bias in terms of the post-legislative scrutiny undertaken thus far, which focuses upon the legislation of the 1997-2010 Labour Governments. There is a strong relationship between the strength of post-legislative recommendations and their acceptance. As a result it is argued that committees deploy a strategy of producing weaker recommendations order to get more of them accepted. Finally, the research finds that while there is evidence of post-legislative scrutiny having impact, there is also untapped potential for further impact should committees in both Houses start following up on their inquiries formally. While there is evidence of post-legislative scrutiny making a difference there is room for improvement in terms of its extent, selection and impact.Economic and Social Research Counci

    Controlling the {111}/{110} Surface Ratio of Cuboidal Ceria Nanoparticles

    Get PDF
    The ability to control size and morphology is crucial in optimizing nanoceria catalytic activity as this is governed by the atomistic arrangement of species and structural features at the surfaces. Here, we show that cuboidal cerium oxide nanoparticles can be obtained via microwave-assisted hydrothermal synthesis in highly alkaline media. HRTEM revealed that the cube edges were truncated by CeO2{110} surfaces and the cube corners by CeO2{111} surfaces. When adjusting synthesis conditions by increasing NaOH concentration, the average particle size increased. Although this was accompanied by an increase of the cube faces, CeO2{100}, the cube edges, CeO2{110}, and cube corners, CeO2{111} remained of constant size. Molecular Dynamics (MD) was used to rationalise this behaviour and revealed that energetically, the corners and edges cannot be atomically sharp, rather they are truncated by {111} and {110} surfaces respectively to stabilise the nanocube; both experiment and simulation agreed a minimum size of ~1.6 nm associated with this truncation. Moreover, HRTEM and MD revealed {111}/{110} faceting of the {110} edges, which balances the surface energy associated with the exposed surfaces, which follows {111}>{110}>{100}, although only the {110} surface facets because of the ease of extracting oxygen from its surface, which follows {111}>{100}>{110}. Finally, MD revealed that the {100} surfaces are ‘liquid-like’ with a surface oxygen mobility 5 orders of magnitude higher than that on the {111} surfaces; this arises from the flexibility of the surface species network that can access many different surface arrangements due to very small energy differences. This finding has implications for understanding the surface chemistry of nanoceria and provides avenues to rationalize the design of catalytically active materials at the nanoscale

    Alteration of EGFR Spatiotemporal Dynamics Suppresses Signal Transduction

    Get PDF
    The epidermal growth factor receptor (EGFR), which regulates cell growth and survival, is integral to colon tumorigenesis. Lipid rafts play a role in regulating EGFR signaling, and docosahexaenoic acid (DHA) is known to perturb membrane domain organization through changes in lipid rafts. Therefore, we investigated the mechanistic link between EGFR function and DHA. Membrane incorporation of DHA into immortalized colonocytes altered the lateral organization of EGFR. DHA additionally increased EGFR phosphorylation but paradoxically suppressed downstream signaling. Assessment of the EGFR-Ras-ERK1/2 signaling cascade identified Ras GTP binding as the locus of the DHA-induced disruption of signal transduction. DHA also antagonized EGFR signaling capacity by increasing receptor internalization and degradation. DHA suppressed cell proliferation in an EGFR-dependent manner, but cell proliferation could be partially rescued by expression of constitutively active Ras. Feeding chronically-inflamed, carcinogen-injected C57BL/6 mice a fish oil containing diet enriched in DHA recapitulated the effects on the EGFR signaling axis observed in cell culture and additionally suppressed tumor formation. We conclude that DHA-induced alteration in both the lateral and subcellular localization of EGFR culminates in the suppression of EGFR downstream signal transduction, which has implications for the molecular basis of colon cancer prevention by DHA

    Modelo de carcinogênese gástrica utilizando piloroplastia de Finney: estudo experimental em ratos Gastric carcinogenesis model using Finney pyloroplasty: experimental study in rats

    No full text
    RACIONAL: O refluxo duodenogástrico tem sido implicado como potencial carcinógeno para o estômago e esôfago e é um dos fatores que podem explicar o desenvolvimento de câncer no coto gástrico. Modelos experimentais de carcinogênese no estômago ressecado ou nas gastrojejunoanastomoses estão bem definidos. OBJETIVOS: Desenvolver um modelo experimental de carcinogênese gástrica através de piloroplastia à Finney, avaliar a influência da ingestão de nitrito de sódio nesse modelo, analisar as concentrações de ácidos biliares e o valor do pH gástrico. MÉTODOS: Foram operados 110 ratos Wistar divididos em quatro grupos: Grupo I (15 ratos) submetidos à laparotomia (grupo Sham); Grupo II (15 ratos) submetidos à laparotomia (Sham) e à ingestão de nitrito de sódio na água de beber; Grupo III (40 ratos) submetidos à piloroplastia à Finney; Grupo IV (40 ratos) submetidos à piloroplastia à Finney e à ingestão de nitrito de sódio na água de beber. Após 50 semanas da operação, os ratos foram sacrificados, coletadas amostras de suco gástrico para análise do pH, dosagem dos ácidos biliares, e realizada análise histológica. RESULTADOS: A mortalidade pós-operatória imediata foi de 9% e, ao longo do experimento, 10 ratos morreram. O grupo controle (I) não apresentou lesões gástricas; o grupo controle com nitrito de sódio (II) desenvolveu papilomas no pré-estômago em 16.6%; os grupos operados com piloroplastia apresentaram adenomas em 10,3% no Grupo III e 14,2% no Grupo IV, e adenocarcinoma em 55,1%, no grupo III e 14,2% no Grupo IV. A implantação de glândulas para dentro da submucosa e muscular, na zona de anastomose (implantação mucosa), não foi critério suficiente para decidir sobre a malignidade das lesões, sendo necessária a presença simultânea de atipias celulares. A concentração de ácidos biliares do suco gástrico foi maior nos Grupos III e IV. A medida do pH gástrico não foi diferente nos grupos estudados. CONCLUSÃO: 1) A piloroplastia à Finney é modelo experimental adequado de carcinogênese gástrica; 2) ela induziu refluxo duodenogástrico; 3) o refluxo duodenogástrico atuou como carcinógeno para o estômago; 4) não houve relação entre o pH gástrico e o desenvolvimento de carcinoma; 5) o nitrito de sódio não atuou como carcinógeno para o estômago dos ratos.<br>BACKGROUND: The duodenogastric reflux has been implicated as a potential carcinogen for the stomach and esophagus and is one of the factors that may explain the development of gastric stump cancer. Experimental models of carcinogenesis in the stomach stump or in the duodenogastric anastomosis are well defined. AIM: To develop an experimental model of gastric carcinogenesis through the Finney pyloroplasty, evaluate the influence of ingestion of sodium nitrite in this model, analyze the concentrations of bile acids and the pH of the stomach. METHODS: A hundred and ten Wistar rats were operated and divided into four groups: Group I (15 rats) underwent laparotomy (Sham group); Group II (15 rats) underwent laparotomy (Sham) and ingestion of sodium nitrite in drinking water; Group III (40 rats) submitted to the Finney pyloroplasty and Group IV (40 rats) submitted to the Finney pyloroplasty and ingestion of sodium nitrite in drinking water. After 50 weeks of surgery, the rats were sacrificed and samples collected for analysis of gastric pH, dosing of bile acids and histological analysis. RESULTS: The immediate postoperative mortality was 9%, and during the experiment, 10 rats died. The control group (I) did not show gastric lesions; the control group with sodium nitrite (II) developed papillomas in the pre-stomach in 16.6%; the operated groups with pyloroplasty had adenomas in 10.3% in Group III and 14.2 % in Group IV, and adenocarcinoma in 55.1% in group III and 14.2% in Group IV. The implementation of glands into the submucosa and muscle in the area of anastomosis (mucosa deployment) was not sufficient criterion for deciding on the malignancy of the lesions, requiring the simultaneous presence of atypical cells. The concentration of bile acids in gastric juice was higher in Groups III and IV. The measurement of gastric pH was not different in both groups. CONCLUSION: 1) The Finney pyloroplasty is suitable experimental model of gastric carcinogenesis; 2) it induced duodenogastric reflux; 3) the duodenogastric reflux served as a carcinogen for the stomach; 4) there was no relationship between pH and the development of gastric carcinoma; 5 ) sodium nitrite did not act as a carcinogen for the stomach of rats
    corecore