Measurement of the CP-violating weak phase φs and the decay width difference δΓc using the Bs 0→J/ψφ(1020) decay channel in pp collisions at √ s=8 TeV

The CP-violating weak phase ϕsϕs of the View the MathML sourceBs0 meson and the decay width difference ΔΓsΔΓs of the View the MathML sourceBs0 light and heavy mass eigenstates are measured with the CMS detector at the LHC using a data sample of View the MathML sourceBs0→J/ψϕ(1020)→μ+μ−K+K− decays. The analysed data set corresponds to an integrated luminosity of View the MathML source19.7fb−1 collected in pp collisions at a centre-of-mass energy of View the MathML source8TeV. A total of 49 200 reconstructed View the MathML sourceBs0 decays are used to extract the values of ϕsϕs and ΔΓsΔΓs by performing a time-dependent and flavour-tagged angular analysis of the μ+μ−K+K−μ+μ−K+K− final state. The weak phase is measured to be View the MathML sourceϕs=−0.075±0.097(stat)±0.031(syst) rad, and the decay width difference is View the MathML sourceΔΓs=0.095±0.013(stat)±0.007(syst) ps−1

Assessment of NADPH-diaphorase stained myenteric neurons of the jejunum of diabetic rats supplemented with ascorbic acid Avaliação dos neurônios NADPH-diaforase reativos do jejuno de raots diabéticos suplementados com ácido ascórbico

The relation between hyperglycemia and diabetic neuropathy has already been demonstrated in some studies. Among the theories proposed for its etiology the oxidative stress stands out. The performance of nitric oxide as a link between the metabolic and vascular neuropathogenic factors that triggers the diabetic neuropathy has already been put forward. This study aimed to assess the quantification and measurements of the cell body profile area (CBPA) of NADPH-diaphorase reactive (NADPH-dp) myenteric neurons of the jejunum of diabetic rats (induced by streptozotocin) supplemented with Ascorbic Acid (AA). These changes in the myenteric neurons seem to be related to the gastrointestinal disturbances observed in diabetes mellitus (DM). Twenty male Wistar rats (Rattus norvegicus) were distributed in 4 groups (n=5): controls (C), control supplemented (CS), diabetic (D), and diabetic suplemented (DS). DM was induced by estreptozotocin (50mg/kg body wt). One week after the induction and confirmation of the DM (glycemia exam), animals of the groups CS and DS received 50mg of AA three times a week by gavage. After 90 days of experiment, the animals were anesthetized with lethal thiopental dose (40mg/kg) and the collected jejunum processed for the histochemistry NADPH-diaphorase technique. Whole-mount preparations were obtained for quantitative and morphometric analysis of the myenteric neurons. A quantity of jejunum neurons in the Group D (96&plusmn;7.5) was not different (P>0.05) from Group DS (116&plusmn;8.08), C (92&plusmn;9.7), and CS (81&plusmn;5.4), but in Group DS the quantity was higher (P<0.05) than in Group C and CS. The CBPA of neurons from Group D (189.50&plusmn;2.68µm²) and DS (195.92&plusmn;3.75µm²) were lower (P<0.05) than from Group C (225.13&plusmn;4.37µm²) and CS (210.23&plusmn;3.15µm²). The streptozotocin-induced DM did not change the jejunum-ileum area, the jejunum myenteric plexus space organization and the density of NADPH-dp neurons. The 50g AA-supplementation, three times a week, during 90 days, did not decrease hyperglycemia; however, it had a neuroprotective effect on the myenteric neurons, minimizing the increase on the CBPA of NADPH-dp neurons and increasing the amount of NADPD-dp neurons.<br>A relação entre hiperglicemia e neuropatia diabética foi demonstrada em várias pesquisas. Entre as teorias propostas para sua etiologia destaca-se o estresse oxidativo. O papel do óxido nítrico como elo entre os fatores neuropatogênicos metabólico e vascular que ativam a neuropatia diabética tem sido ressaltado. Este estudo objetivou avaliar a quantificação e a morfometria da área do perfil do corpo celular (CBPA) de neurônios mioentéricos NADPH-diaforase reativos (NADPH-dp) do jejuno de ratos diabéticos e suplementados com Ácido Ascórbico (AA), uma vez que alterações nos neurônios mioentéricos parecem estar relacionadas aos distúrbios gastrointestinais observados no diabetes mellitus (DM). Vinte ratos machos da linhagem Wistar (Rattus norvergicus) foram distribuídos em 4 grupos (n=5): controle (C), controle suplementado (CS), diabético (D) e diabético suplementado (DS). O DM foi induzido através de injeção de estreptozootocina (50mg/kg de peso corporal). Uma semana depois da indução e confirmação do DM (glicemia), animais dos grupos CS e DS receberam, via gavagem, 50mg de AA três vezes por semana. Após 90 dias de período experimental, os animais foram anestesiados com dose letal de thiopental intravenosa (40mg/kg) e o jejuno foi retirado e processado para a técnica histoquímica da NADPH-diaforase. Preparados de membrana foram obtidos para análises quantitativa e morfométrica dos neurônios mioentéricos. A quantidade de neurônios do jejuno do Grupo D (96&plusmn;7,5) não diferiu (P>0,05) dos Grupos DS (116&plusmn;8,08), C (92&plusmn;9,7) e CS (81&plusmn;5,4), mas no Grupo DS o número de neurônios foi superior (P<0,05) aos Grupos C e CS. A CBPA de neurônios do Grupo D (189,50&plusmn;2,68µm²) e DS (195,92&plusmn;3,75µm²) foi menor (P<0,05) do que a dos Grupos C (225,13&plusmn;4,37µm²) e CS (210,23&plusmn;3,15µm²). O DM induzido por estreptozootocina não alterou a área do jejuno-íleo, a organização espacial do plexo mioentérico e a densidade de neurônios de NADPH-dp do jejuno. A suplementação de 50mg de AA, três vezes por semana, durante 90 dias, não diminuiu a hiperglicemia, porém teve efeito neuroprotetor nos neurônios mioentéricos, minimizando o aumento na CBPA dos neurônios NADPH-dp e aumentando a quantidade de neurônios reativos a NADPD-diaforase

Dialectics of Counting and the Mathematics of Vagueness

Abstract. New concepts of rough natural number systems are intro-duced in this research paper from both formal and less formal perspec-tives. These are used to improve most rough set-theoretical measures in general Rough Set theory (RST) and to represent rough semantics. The foundations of the theory also rely upon the axiomatic approach to granularity for all types of general RST recently developed by the present author. The latter theory is expanded upon in this paper. It is also shown that algebraic semantics of classical RST can be obtained from the developed dialectical counting procedures. Fuzzy set theory is also shown to be representable in purely granule-theoretic terms in the general perspective of solving the contamination problem that pervades this research paper. All this constitutes a radically different approach to the mathematics of vague phenomena and suggests new directions for a more realistic extension of the foundations of mathematics of vagueness from both foundational and application points of view. Algebras corre-sponding to a concept of rough naturals are also studied and variants are characterised in the penultimate section

Meta-analysis of Genome-wide Association Studies for Neuroticism, and the Polygenic Association With Major Depressive Disorder

IMPORTANCE Neuroticism is a pervasive risk factor for psychiatric conditions. It genetically overlaps with major depressive disorder (MDD) and is therefore an important phenotype for psychiatric genetics. The Genetics of Personality Consortium has created a resource for genome-wide association analyses of personality traits in more than 63 000 participants (including MDD cases). OBJECTIVES To identify genetic variants associated with neuroticism by performing a meta-analysis of genome-wide association results based on 1000 Genomes imputation; to evaluate whether common genetic variants as assessed by single-nucleotide polymorphisms (SNPs) explain variation in neuroticism by estimating SNP-based heritability; and to examine whether SNPs that predict neuroticism also predict MDD. DESIGN, SETTING, AND PARTICIPANTS Genome-wide association meta-analysis of 30 cohorts with genome-wide genotype, personality, and MDD data from the Genetics of Personality Consortium. The study included 63 661 participants from 29 discovery cohorts and 9786 participants from a replication cohort. Participants came from Europe, the United States, or Australia. Analyses were conducted between 2012 and 2014. MAIN OUTCOMES AND MEASURES Neuroticism scores harmonized across all 29 discovery cohorts by item response theory analysis, and clinical MDD case-control status in 2 of the cohorts. RESULTS A genome-wide significant SNP was found on 3p14 in MAGI1 (rs35855737; P = 9.26 × 10-9 in the discovery meta-analysis). This association was not replicated (P = .32), but the SNP was still genome-wide significant in the meta-analysis of all 30 cohorts (P = 2.38 × 10-8). Common genetic variants explain 15%of the variance in neuroticism. Polygenic scores based on the meta-analysis of neuroticism in 27 cohorts significantly predicted neuroticism (1.09 × 10-12 < P <.05) and MDD (4.02 × 10-9 < P < .05) in the 2 other cohorts. CONCLUSIONS AND RELEVANCE This study identifies a novel locus for neuroticism. The variant is located in a known gene that has been associated with bipolar disorder and schizophrenia in previous studies. In addition, the study shows that neuroticism is influenced by many genetic variants of small effect that are either common or tagged by common variants. These genetic variants also influence MDD. Future studies should confirm the role of the MAGI1 locus for neuroticism and further investigate the association of MAGI1 and the polygenic association to a range of other psychiatric disorders that are phenotypically correlated with neuroticism