Last Province Aboard: New Brunswick and National Medicare

Introduced as a federal-provincial cost-sharing program in the 1960s, medicare aligned ideologically with Premier Louis J. Robichaud’s Equal Opportunity program. New Brunswick was one of the first Canadian provinces to support the adoption of universal healthcare, but it was the last province to implement medicare. This article examines the federal-provincial negotiations surrounding medicare in order to shed light on the scope of Robichaud’s program of Equal Opportunity, to re-evaluate the last years of the Robichaud administration, and to explore why the Progressive Conservative government of Richard Hatfield was responsible for the implementation of medicare in New Brunswick.Le régime d’assurance-maladie, introduit dans les années 1960 comme un programme fédéral-provincial à coûts partagés, était conforme à l’idéologie du programme « Chances égales pour tous » du premier ministre Louis J. Robichaud. Le Nouveau-Brunswick fut l’une des premières provinces canadiennes à appuyer l’adoption de l’assurance-maladie universelle, mais il fut la dernière province à la mettre en œuvre. Cet article examine les négociations fédérales-provinciales entourant le programme d’assurance-maladie en vue de jeter un nouvel éclairage sur la portée du programme « Chances égales » de Robichaud, de réévaluer les dernières années de l’administration Robichaud et d’explorer pourquoi c’est le gouvernement progressiste-conservateur de Richard Hatfield qui fut responsable de la mise en œuvre de l’assurance-maladie au Nouveau-Brunswick

Investigation of Hypersonic Nozzle Flow Uniformity Using NO Fluorescence

Planar laser-induced fluorescence visualisation is used to investigate nonuniformities in the flow of a hypersonic conical nozzle. Possible causes for the nonuniformity are outlined and investigated, and the problem is shown to be due to a small step at the nozzle throat. Entrainment of cold boundary layer gas is postulated as the cause of the signal nonuniformity

The radius and mass of the subgiant star bet Hyi from interferometry and asteroseismology

We have used the Sydney University Stellar Interferometer (SUSI) to measure the angular diameter of beta Hydri. This star is a nearby G2 subgiant whose mean density was recently measured with high precision using asteroseismology. We determine the radius and effective temperature of the star to be 1.814+/-0.017 R_sun (0.9%) and 5872+/-44 K (0.7%) respectively. By combining this value with the mean density, as estimated from asteroseismology, we make a direct estimate of the stellar mass. We find a value of 1.07+/-0.03 M_sun (2.8%), which agrees with published estimates based on fitting in the H-R diagram, but has much higher precision. These results place valuable constraints on theoretical models of beta Hyi and its oscillation frequencies.Comment: 3 figures, 3 tables, to appear in MNRAS Letter

Examination of thromboxane synthase as a prognostic factor and therapeutic target in non-small cell lung cancer

Background: Thromboxane synthase (TXS) metabolises prostaglandin H2 into thromboxanes, which are biologically active on cancer cells. TXS over-expression has been reported in a range of cancers, and associated with a poor prognosis. TXS inhibition induces cell death in-vitro, providing a rationale for therapeutic intervention. We aimed to determine the expression profile of TXS in NSCLC and if it is prognostic and/or a survival factor in the disease. Methods: TXS expression was examined in human NSCLC and matched controls by western analysis and IHC. TXS metabolite (TXB 2) levels were measured by EIA. A 204-patient NSCLC TMA was stained for COX-2 and downstream TXS expression. TXS tissue expression was correlated with clinical parameters, including overall survival. Cell proliferation/survival and invasion was examined in NSCLC cells following both selective TXS inhibition and stable TXS over-expression. Results: TXS was over-expressed in human NSCLC samples, relative to matched normal controls. TXS and TXB 2levels were increased in protein (p < 0.05) and plasma (p < 0.01) NSCLC samples respectively. TXS tissue expression was higher in adenocarcinoma (p < 0.001) and female patients (p < 0.05). No significant correlation with patient survival was observed. Selective TXS inhibition significantly reduced tumour cell growth and increased apoptosis, while TXS over-expression stimulated cell proliferation and invasiveness, and was protective against apoptosis. Conclusion: TXS is over-expressed in NSCLC, particularly in the adenocarcinoma subtype. Inhibition of this enzyme inhibits proliferation and induces apoptosis. Targeting thromboxane synthase alone, or in combination with conventional chemotherapy is a potential therapeutic strategy for NSCLC. © 2011 Cathcart et al; licensee BioMed Central Ltd

Amino acids other than glutamate affect the expression of the GAD system in Listeria monocytogenes enhancing acid resistance

The Glutamate Decarboxylase (GAD) system is important for survival of L. monocytogenes and other microorganisms under acidic conditions. Environmental conditions influence the function of the GAD system. Until now, the only conditions known to lead to increased transcription of the GAD system are the stationary phase in rich media and anoxic conditions. Previously, we showed that transcription of the GAD system requires unidentified compounds other than glutamate present in rich media. Following a test looking at various compounds we identified for first time that peptone, tryptone and casamino acids activate the GAD system under oxic conditions suggesting that amino acid(s) other than glutamate and/or peptides are important for the above process. The defined medium, where the GAD system is inactive, once it is supplemented with the above compounds results in an active intracellular and extracellular GAD system and increased acid resistance. Through functional genomics we show that these compounds are required for GadD2 activity and although we previously showed that GadD3 is active part of the intracellular GAD system, the supplementation did not activate this gene. The above is explained by the fact that only gadD2 transcription was upregulated by these compounds while the transcription of gadD1 and gadD3 remained unaffected. Together our results show that the L. monocytogenes GadD2 decarboxylase is activated in the presence of amino acids or peptides other than glutamate, a finding that has important implications for acid tolerance and food safety

The Vibrio parahaemolyticus Type III Secretion Systems manipulate host cell MAPK for critical steps in pathogenesis

<p>Abstract</p> <p>Background</p> <p><it>Vibrio parahaemolyticus </it>is a food-borne pathogen causing inflammation of the gastrointestinal epithelium. Pathogenic strains of this bacterium possess two Type III Secretion Systems (TTSS) that deliver effector proteins into host cells. In order to better understand human host cell responses to <it>V. parahaemolyticus</it>, the modulation of Mitogen Activated Protein Kinase (MAPK) activation in epithelial cells by an O3:K6 clinical isolate, RIMD2210633, was investigated. The importance of MAPK activation for the ability of the bacterium to be cytotoxic and to induce secretion of Interleukin-8 (IL-8) was determined.</p> <p>Results</p> <p><it>V. parahaemolyticus </it>deployed its TTSS1 to induce activation of the JNK, p38 and ERK MAPK in human epithelial cells. VP1680 was identified as the TTSS1 effector protein responsible for MAPK activation in Caco-2 cells and the activation of JNK and ERK by this protein was important in induction of host cell death. <it>V. parahaemolyticus </it>actively induced IL-8 secretion in a response mediated by TTSS1. A role for VP1680 and for the ERK signalling pathway in the stimulation of IL-8 production in epithelial cells by <it>V. parahaemolyticus </it>was established. Interestingly, TTSS2 inhibited IL-8 mRNA transcription at early stages of interaction between the bacterium and the cell.</p> <p>Conclusions</p> <p>This study demonstrated that <it>V. parahaemolyticus </it>activates the three major MAPK signalling pathways in intestinal epithelial cells in a TTSS1-dependent manner that involves the TTSS1 effector VP1680. Furthermore VP1680 and JNK and ERK activation were needed for maximal cytotoxicity of the bacterium. It was shown that <it>V. parahaemolyticus </it>is a strong inducer of IL-8 secretion and that induction reflects a balance between the effects of TTSS1 and TTSS2. Increases in IL-8 secretion were mediated by TTSS1 and VP1680, and augmented by ERK activation. These results shed light on the mechanisms of bacterial pathogenesis mediated by TTSS and suggest significant roles for MAPK signalling during infection with <it>V. parahaemolyticus</it>.</p