936 research outputs found

    Poisson brackets symmetry from the pentagon-wheel cocycle in the graph complex

    Get PDF
    Kontsevich designed a scheme to generate infinitesimal symmetries P˙=Q(P)\dot{\mathcal{P}} = \mathcal{Q}(\mathcal{P}) of Poisson brackets P\mathcal{P} on all affine manifolds MrM^r; every such deformation is encoded by oriented graphs on n+2n+2 vertices and 2n2n edges. In particular, these symmetries can be obtained by orienting sums of non-oriented graphs γ\gamma on nn vertices and 2n22n-2 edges. The bi-vector flow P˙=Or(γ)(P)\dot{\mathcal{P}} = \text{Or}(\gamma)(\mathcal{P}) preserves the space of Poisson structures if γ\gamma is a cocycle with respect to the vertex-expanding differential in the graph complex. A class of such cocycles γ2+1\boldsymbol{\gamma}_{2\ell+1} is known to exist: marked by N\ell \in \mathbb{N}, each of them contains a (2+1)(2\ell+1)-gon wheel with a nonzero coefficient. At =1\ell=1 the tetrahedron γ3\boldsymbol{\gamma}_3 itself is a cocycle; at =2\ell=2 the Kontsevich--Willwacher pentagon-wheel cocycle γ5\boldsymbol{\gamma}_5 consists of two graphs. We reconstruct the symmetry Q5(P)=Or(γ5)(P)\mathcal{Q}_5(\mathcal{P}) = \text{Or}(\boldsymbol{\gamma}_5)(\mathcal{P}) and verify that Q5\mathcal{Q}_5 is a Poisson cocycle indeed: [ ⁣[P,Q5(P)] ⁣]0[\![\mathcal{P},\mathcal{Q}_5(\mathcal{P})]\!]\doteq 0 via [ ⁣[P,P] ⁣]=0[\![\mathcal{P},\mathcal{P}]\!]=0.Comment: Int. workshop "Supersymmetries and quantum symmetries -- SQS'17" (July 31 -- August 5, 2017 at JINR Dubna, Russia), 4+v pages, 2 figures, 1 tabl

    A polymorphism in the 3' untranslated region of the gene encoding prostaglandin endoperoxide synthase 2 is not associated with an increase in breast cancer risk: a nested case-control study

    Get PDF
    INTRODUCTION: Prostaglandins are integral components in the cellular response to inflammation, promoting cellular proliferation and angiogenesis. The enzyme responsible for the conversion of arachidonic acid to prostaglandins in response to inflammation is prostaglandin endoperoxide synthase 2/cyclo-oxygenase 2 (PTGS2/COX2). Polymorphisms in the PTGS2 gene have been associated with various diseases, including inflammatory bowel disease and cancer of the lung, colorectum, and breast. METHODS: We genotyped the five most common polymorphisms (rs20417, rs5277, rs20432, rs5275, and rs4648298) in the Nurses' Health Study (1,270 cases, 1,762 controls) to test the hypothesis that polymorphisms in PTGS2 are associated with breast cancer risk, using logistic regression analyses. The Nurses' Health Study 2 (317 cases, 634 controls) and Harvard Women's Health Study (702 cases, 703 controls) were used to further examine putative associations. RESULTS: The rs5275 polymorphism in the 3' untranslated region of the PTGS2 gene was associated with a decrease in breast cancer risk. We therefore genotyped this single-nucleotide polymorphism in the Nurses' Health Study 2 and Harvard Women's Health Study. Similar results were observed in these subsequent analyses, with no statistically significant heterogeneity in risk estimates between studies. In pooled analyses, women homozygous for the T allele at rs5275 had a 20% lower risk of breast cancer than those homozygous for the C allele (odds ratio 0.80, 95% confidence interval 0.66 to 0.97). CONCLUSION: Although this polymorphism may be associated with a decrease in breast cancer risk among Caucasian women, we provide strong evidence that it is not associated with an increased risk of breast cancer

    Migraine, vascular risk, and cardiovascular events in women: prospective cohort study

    Get PDF
    Objectives To evaluate whether the association between migraine with aura and increased risk of cardiovascular disease is modified by vascular risk groups as measured by the Framingham risk score for coronary heart disease

    Socioeconomic status, blood pressure progression, and incident hypertension in a prospective cohort of female health professionals

    Get PDF
    Aims The aim of this study was to examine the association between socioeconomic status, blood pressure (BP) progression, and incident hypertension. Methods and results We included 27 207 female health professionals free of hypertension and cardiovascular disease at baseline. Participants were classified into five education and six income categories. The main outcome variables were BP progression at 48 months of follow-up and incident hypertension during the entire study period. At 48 months, 48.1% of women had BP progression. The multivariable adjusted relative risks [95% confidence intervals (CIs)] for BP progression were 1.0 (referent), 0.96 (0.92-1.00), 0.92 (0.88-0.96), 0.90 (0.85-0.94), and 0.84 (0.78-0.91) (P for trend <0.0001) across increasing education categories and 1.0 (referent), 1.01 (0.94-1.08), 0.99 (0.93-1.06), 0.97 (0.91-1.04), 0.96 (0.90-1.03), and 0.89 (0.83-0.96) across increasing income categories (P for trend = 0.0001). During a median follow-up of 9.8 years, 8248 cases of incident hypertension occurred. Multivariable adjusted hazard ratios (95% CI) were 1.0 (referent), 0.92 (0.86-0.99), 0.85 (0.79-0.92), 0.87 (0.80-0.94), and 0.74 (0.65-0.84) (P for trend <0.0001) across increasing education categories and 1.0 (referent), 1.07 (0.95-1.21), 1.07 (0.95-1.20), 1.06 (0.94-1.18), 1.04 (0.93-1.16), and 0.93 (0.82-1.06) (P for trend 0.08) across increasing income categories. In joint analyses, education but not income remained associated with BP progression and incident hypertension. Conclusion Socioeconomic status, as determined by education but not by income, is a strong independent predictor of BP progression and incident hypertension in wome

    The Mitochondrial A10398G Polymorphism, Interaction with Alcohol Consumption, and Breast Cancer Risk

    Get PDF
    Polymorphisms in the mitochondrial genome are hypothesized to be associated with risk of various diseases, including cancer. However, there has been conflicting evidence for associations between a common polymorphism in the mitochondrial genome (A10398G, G10398A in some prior reports) and breast cancer risk. Reactive oxygen species, a by-product of mitochondrial energy production, can lead to oxidative stress and DNA damage in both the mitochondria and their cells. Alcohol consumption, which may also lead to oxidative stress, is associated with breast cancer risk. Therefore, we hypothesized that polymorphisms in the mitochondrial genome interact with alcohol consumption to alter breast cancer risk. We genotyped the A10398G polymorphism in a case-control study nested within the Nurses' Health Study (NHS, 1,561 cases, 2,209 controls). We observed an interaction between alcohol consumption (yes/no) and A10398G on breast cancer risk (p-int = 0.03). The risk associated with alcohol consumption was limited to carriers of the 10398G allele (Odds Ratio 1.52, 95% Confidence Interval 1.10–2.08 comparing drinkers to non-drinkers). However, we were unable to replicate these findings in the Women's Health Study (WHS, 678 cases, 669 controls), although the power to detect this interaction in the WHS was low (power = 0.57). Further examination of this interaction, such as sufficiently powered epidemiological studies of cancer risk or associations with biomarkers of oxidative stress, may provide further evidence for GxE interactions between the A10398G mitochondrial polymorphism and alcohol consumption on breast cancer risk
    corecore