A New Three-Algebra Representation for the {\cal N}=6 su(N)Xsu(N) Superconformal Chern-Simons Theory

Based on the realization of three-algebras in terms of algebra of matrices and four-brackets [arXiv:0807.1570] we present the notion of u(N)-based extended three-algebras, which for N=2 reproduces the Bagger-Lambert three-algebra. Using these extended three-algebras we construct an su(N)\times su(N) Chern-Simons action with explicit SO(8) invariance. The dynamical fields of this theory are eight complex valued bosonic and fermionic fields in the bi-fundamental representation of the su(N)\times su(N). For generic N the fermionic transformations, however, close only on a subclass of the states of this theory onto the 3d, {\cal N}=6 superalgebra. In this sector we deal with four complex valued scalars and fermions, our theory is closely related to the ABJM model [arXiv:0806.1218], and hence it can be viewed as the (low energy effective) theory of N M2-branes. We discuss that our three-algebra structure suggests a picture of open M2-brane stretched between any two pairs of M2-branes. We also analyze the BPS configurations of our model.Comment: 39 pages, 3 .eps figures, v2: References added, typos corrected, v3: typos corrected, an appendix added, the version to appear in JHE

Clinical And Neuropsychological Correlation In Patients With Rolandic Epilepsy [correlação Entre Achados Clínicos E Neuropsicológicos Em Pacientes Com Epilepsia Rolândica]

Objectives: To evaluate the presence of neurological soft signs (NSS) and to correlate them with the Wechsler Intelligence Scale for Children (WISC III) in patients with rolandic epilepsy (RE). Methods: Forty children and adolescents aged between 9 and 15 years were studied. They were divided into two groups: G1 - patients with RE (n=20) - and G2 - healthy controls without epilepsy (n=20). They were assessed with the Quick Neurological Screening Test (QNST II) - clinical trial to search for NSS -, and the WISC III - neuropsychological test. Results: No statistical difference between groups was found in WISC III and QNST II. However, children with poorer motor skills had worse performance in the QNST II and also in the execution intelligence quotient - IQ (p=0.001) and in total IQ (p=0.004), thus showing a positive correlation between them. Conclusions: The QNST II is a good screening tool for the neurologist to detect abnormalities in fine motor skills.709691693Berg, A.T., Berkovic, S.F., Brodie, M.J., Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005-2009 (2010) Epilepsia, 51, pp. 676-685Lerman, P., Kivity, S., Benign focal epilepsy of childhood. A follow-up study of 100 recovered patients (1975) Arch Neurol, 32, pp. 261-264Bouma, P.A., Bovenkerk, A.C., Westendorp, R.G., Brouwer, O.F., The course of benign partial epilepsy of childhood with centrotemporal spikes: A meta-analysis (1997) Neurology, 48 (2), pp. 430-437Hommet, C., Billard, C., Motte, J., Cognitive function in adolescents and young adults in complete remission from benign childhood epilepsy with centro-temporal spikes (2001) Epileptic Disord, 3, pp. 207-216D'Alessandro, P., Piccirilli, M., Tiacci, C., Neuropsychological features of benign partial epilepsy in children (1990) Ital J Neurol Sci, 11, pp. 265-269Binnie, C.D., Marston, D., Cognitive correlates of interictal discharges (1992) Epilepsia, 33 (SUPPL. 6), pp. S11-S17Fonseca, L.C., Tedrus, G.M., Pacheco, E.M., Epileptiform EEG discharges in benign childhood epilepsy with centrotemporal spikes: Reactivity and transitory cognitive impairment (2007) Epilepsy Behav, 11, pp. 65-70Baglietto, M.G., Battaglia, F.M., Nobili, N., Neuropsychological disorders related to interictal epileptic discharges during sleep in benign epilepsy of childhood with centrotemporal or rolandic spikes (2001) Dev Med Child Neurol, 43, pp. 407-412Hermann, B.P., Jones, J., Sheth, R., Seidenberg, M., Cognitive and magnetic resonance volumetric abnormalities in new-onset pediatric epilepsy (2007) Semin Pediatri Neurol, 14, pp. 173-180Panayiotopoulos, C.P., Benign childhood partial epilepsies: Benign childhood seizures susceptibility syndromes (1993) J Neurol Neurosurg Psychiatry, 56, pp. 2-5Lindgren, A., Kihlgren, M., Melin, L., Croona, C., Development of cognitive functions in children with rolandic epilepsy (2004) Epilepsy Behav, 5, pp. 903-910Weglage, J., Demsky, A., Pietsh, M., Kurlemann, G., Neuropsychological, intellectual, and behavioral findings in patients with centrotemporal spikes with and without seizure (1997) Dev Med Child Neurol, 39, pp. 645-651Deonna, T., Rolandic epilepsy: Neuropsychology of the active epilepsy phase (2000) Epileptic Disord, 2 (SUPPL. 1), pp. S59-S61Deonna, T., Zesiger, P., Davidoff, V., Benign partial epilepsy of childhood: A longitudinal neuropsychological and EEG study of cognitive function (2000) Dev Med Child Neurol, 42, pp. 595-60

Identification and pathogenicity of Macrophomina species collected from weeds in melon fields in Northeastern Brazil

"This is the peer reviewed version of the following article: Negreiros, AMP, Sales Júnior, R, León, M, et al. Identification and pathogenicity of Macrophomina species collected from weeds in melon fields in Northeastern Brazil. J Phytopathol. 2019; 167: 326 337. , which has been published in final form at https://doi.org/10.1111/jph.12801. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving."[EN] In this work, a collection of 94 Macrophomina isolates obtained from roots of two weed species, Trianthema portulacastrum and Boerhavia diffusa, collected during surveys conducted during 2015 and 2016 in melon production fields in Northeastern Brazil, were characterized by using molecular techniques. Phylogenetic analysis of the EF1-alpha gene allowed the identification of 32 isolates as M. phaseolina and 62 isolates as M. pseudophaseolina. Results of a pathogenicity test performed on melon seedlings of the cv. "Gladial" revealed that all M. phaseolina isolates inoculated were able to cause disease to melon seedlings, but only some M. pseudophaseolina isolates were able to infect them. This study represents the first report of M. pseudophaseolina in both T. portulacastrum and B. diffusa weeds, which are prevalent in the main Brazilian melon producing and exporting regions. Information about the biology and epidemiology of M. pseudophaseolina is scarce because of its recent description; thus, further research is needed for a better understanding of this fungus as a potentially emerging pathogen of melon and other crops.Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior-Brazil (CAPES); Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Negreiros, AMP.; Sales Junior, R.; León Santana, M.; de Assis Melo N.J.; Michereff, S.; de Queiroz Ambrósio M.M.; De Sousa Medeiros, H.... (2019). Identification and pathogenicity of Macrophomina species collected from weeds in melon fields in Northeastern Brazil. Journal of Phytopathology. 167(6):326-337. https://doi.org/10.1111/jph.12801S3263371676Agustí-Brisach, C., Gramaje, D., León, M., García-Jiménez, J., & Armengol, J. (2011). Evaluation of Vineyard Weeds as Potential Hosts of Black-Foot and Petri Disease Pathogens. Plant Disease, 95(7), 803-810. doi:10.1094/pdis-12-10-0888A. C. Alfenas R. Mafia G. Métodos em fitopatologia 2016 Ed. UFV Universidade Federal de Viçosa Viçosa Brasil 516Ambrósio, M. M. Q., Dantas, A. C. A., Martínez-Perez, E., Medeiros, A. C., Nunes, G. H. S., & Picó, M. B. (2015). Screening a variable germplasm collection of Cucumis melo L. for seedling resistance to Macrophomina phaseolina. Euphytica, 206(2), 287-300. doi:10.1007/s10681-015-1452-xAnuário Anuário ‐ Anuário Brasileiro da Fruticultura 2018 2018 Ed. Gazeta Santa Cruz Santa Cruz do Sul Brazil 88Baird, R. E., & Brock, J. H. (1999). First Report of Macrophomina phaseolina on Cotton (Gossypium hirsutum) in Georgia. Plant Disease, 83(5), 487-487. doi:10.1094/pdis.1999.83.5.487bBaird, R. E., Watson, C. E., & Scruggs, M. (2003). Relative Longevity of Macrophomina phaseolina and Associated Mycobiota on Residual Soybean Roots in Soil. Plant Disease, 87(5), 563-566. doi:10.1094/pdis.2003.87.5.563Carbone, I., & Kohn, L. M. (1999). A Method for Designing Primer Sets for Speciation Studies in Filamentous Ascomycetes. Mycologia, 91(3), 553. doi:10.2307/3761358Chaves, A. L. R., Braun, M. R., Eiras, M., Colariccio, A., & Galleti, S. R. (2003). Erigeron bonariensis: hospedeira alternativa do Lettuce mosaic virus no Brasil. Fitopatologia Brasileira, 28(3), 307-311. doi:10.1590/s0100-41582003000300014Claudino, M. R., & Soares, D. J. (2014). Pathogenicity and aggressiveness of Macrophomina phaseolina isolates to castor (Ricinus communis). Tropical Plant Pathology, 39(6), 453-456. doi:10.1590/s1982-56762014000600006Cohen, R., Omari, N., Porat, A., & Edelstein, M. (2012). Management of Macrophomina wilt in melons using grafting or fungicide soil application: Pathological, horticultural and economical aspects. Crop Protection, 35, 58-63. doi:10.1016/j.cropro.2011.12.015FAOSTAT(2018). FAO statistical databases food and agriculture organization of the United Nations.http://www.fao.org/faostat/en/#home.Farr D. F. &Rossman A. Y.(2018). Fungal Databases. National Fungus Collections ARS USDA: U.S.https://nt.ars-grin.gov/fungaldatabases/.Fuhlbohm, M. J., Ryley, M. J., & Aitken, E. A. B. (2012). New weed hosts of Macrophomina phaseolina in Australia. Australasian Plant Disease Notes, 7(1), 193-195. doi:10.1007/s13314-012-0082-6Funnell-Harris, D. L., O’Neill, P. M., Sattler, S. E., & Yerka, M. K. (2016). Response of Sweet Sorghum Lines to Stalk Pathogens Fusarium thapsinum and Macrophomina phaseolina. Plant Disease, 100(5), 896-903. doi:10.1094/pdis-09-15-1050-reIBGE(2018). Instituto Brasileiro de Geografia e Estatística.https://sidra.ibge.gov.br/home/pms/brasil.Jacob, C. J., Krarup, C., Díaz, G. A., & Latorre, B. A. (2013). A Severe Outbreak of Charcoal Rot in Cantaloupe Melon Caused by Macrophomina phaseolina in Chile. Plant Disease, 97(1), 141-141. doi:10.1094/pdis-06-12-0588-pdnKumar, S., Stecher, G., & Tamura, K. (2016). MEGA7: Molecular Evolutionary Genetics Analysis Version 7.0 for Bigger Datasets. Molecular Biology and Evolution, 33(7), 1870-1874. doi:10.1093/molbev/msw054Machado, A. R., Pinho, D. B., & Pereira, O. L. (2014). Phylogeny, identification and pathogenicity of the Botryosphaeriaceae associated with collar and root rot of the biofuel plant Jatropha curcas in Brazil, with a description of new species of Lasiodiplodia. Fungal Diversity, 67(1), 231-247. doi:10.1007/s13225-013-0274-1Machado, A. R., Pinho, D. B., Soares, D. J., Gomes, A. A. M., & Pereira, O. L. (2018). Bayesian analyses of five gene regions reveal a new phylogenetic species of Macrophomina associated with charcoal rot on oilseed crops in Brazil. European Journal of Plant Pathology, 153(1), 89-100. doi:10.1007/s10658-018-1545-1Medeiros, A. C., Melo, D. R. M. de, Ambrósio, M. M. de Q., Nunes, G. H. de S., & Costa, J. M. da. (2015). Métodos de inoculação de Rhizoctonia solani e Macrophomina phaseolina em meloeiro (Cucumis melo). Summa Phytopathologica, 41(4), 281-286. doi:10.1590/0100-5405/2083Miller M. A. Pfeiffer W. &Schwartz T.(2012). The CIPRES science gateway: enabling high‐impact science for phylogenetics researchers with limited resources. In: Proceedings of the 1st Conference of the Extreme Science and Engineering Discovery Environment: Bridging from the extreme to the campus and beyond (pp.39).Chicago IL.Mir, Z. R., Singh, P. K., Zaidi, P. H., Vinayan, M. T., Sharma, S. S., Krishna, M. K., … Nair, S. K. (2018). Genetic analysis of resistance to post flowering stalk rot in tropical germplasm of maize ( Zea mays L.). Crop Protection, 106, 42-49. doi:10.1016/j.cropro.2017.12.004Mbaye, N., Mame, P. S., Ndiaga, C., & Ibrahima, N. (2015). Is the recently described Macrophomina pseudophaseolina pathogenically different from Macrophomina phaseolina? African Journal of Microbiology Research, 9(45), 2232-2238. doi:10.5897/ajmr2015.7742Nylander J. A. A.(2004). MrModeltest V2. Program Distributed by the Author: Evolutionary Biology Centre Uppsala University Sweden.Reuveni, R., Krikun, J., Nachmias, A., & Shlevin, E. (1982). The role ofMacrophomina phaseolina in a collapse of melon plants in Israel. Phytoparasitica, 10(1), 51-56. doi:10.1007/bf02981892Ronquist, F., Teslenko, M., van der Mark, P., Ayres, D. L., Darling, A., Höhna, S., … Huelsenbeck, J. P. (2012). MrBayes 3.2: Efficient Bayesian Phylogenetic Inference and Model Choice Across a Large Model Space. 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On the influence of a Coulomb-like potential induced by the Lorentz symmetry breaking effects on the Harmonic Oscillator

In this work, we obtain bound states for a nonrelativistic spin-half neutral particle under the influence of a Coulomb-like potential induced by the Lorentz symmetry breaking effects. We present a new possible scenario of studying the Lorentz symmetry breaking effects on a nonrelativistic quantum system defined by a fixed space-like vector field parallel to the radial direction interacting with a uniform magnetic field along the z-axis. Furthermore, we also discuss the influence of a Coulomb-like potential induced by Lorentz symmetry violation effects on the two-dimensional harmonic oscillator.Comment: 14 pages, no figure, this work has been accepted for publication in The European Physical Journal Plu

Aerobic exercise prevents cardiomyocyte damage caused by oxidative stress in early cardiovascular disease by increasing vascularity while L-arginine supplementation prevents it by increasing activation of the enzyme nitric oxide synthase

L-Arginine and chronic exercise reduce oxidative stress. However, it is unclear how they affect cardiomyocytes during cardiovascular disease (CVD) development. The aim of this research was to investigate the possible effects of L-arginine supplementation and aerobic training on systemic oxidative stress and their consequences on cardiomyocytes during cardiometabolic disease onset caused by excess fructose. Wistar rats were allocated into four groups: control (C), fructose (F, 10% fructose in water), fructose training (FT; moderate running, 50-70% of the maximal velocity), and fructose arginine (FA; 880 mg/kg/day). Fructose was given for two weeks and fructose plus treatments for the subsequent eight weeks. Body composition, blood glucose, insulin, lipid profile, lipid peroxidation, nitrite, metalloproteinase-2 (MMP-2) activity, left ventricle histological changes, microRNA-126, -195, and -146, eNOS, p-eNOS, and TNF-α expressions were analyzed. Higher abdominal fat mass, triacylglycerol level, and insulin level were observed in the F group, and both treatments reversed these alterations. Myocardial vascularization was impaired in fructose-fed groups, except in FT. Cardiomyocyte hypertrophy was observed in all fructose-fed groups. TNF-α levels were higher in fructose-fed groups than in the C group, and p-eNOS levels were higher in the FA than in the C and F groups. Lipid peroxidation was higher in the F group than in the FT and C groups. During CVD onset, moderate aerobic exercise reduced lipid peroxidation, and both training and L-arginine prevented metabolic changes caused by excessive fructose. Myocardial vascularization was impaired by fructose, and cardiomyocyte hypertrophy appeared to be influenced by pro-inflammatory and oxidative environments