Consenso mexicano sobre dolor torácico no cardiaco

Introducción: Dolor torácico no cardíaco (DTNC) se define como un síndrome clínico caracte-rizado por dolor retroesternal semejante a la angina de pecho, pero de origen no cardiaco ygenerado por enfermedades esofágicas, osteomusculares, pulmonares o psiquiátricas.Objetivo: Presentar una revisión consensuada basada en evidencias sobre definición, epidemio-logía, fisiopatología, diagnóstico y opciones terapéuticas para pacientes con DTNC.Métodos: Tres coordinadores generales realizaron una revisión bibliográfica de todas las publi-caciones en inglés y espa˜nol sobre el tema y elaboraron 38 enunciados iniciales divididosen tres categorías principales: 1) definiciones, epidemiología y fisiopatología; 2) diagnóstico,y 3) tratamiento. Los enunciados fueron votados (3 rondas) utilizando el sistema Delphi, y losque alcanzaron un acuerdo > 75% fueron considerados y calificados de acuerdo con el sistemaGRADE. Resultados y conclusiones: El consenso final incluyó 29 enunciados Todo paciente que debutacon dolor torácico debe ser inicialmente evaluado por un cardiólogo. La causa más común deDTNC es la enfermedad por reflujo gastroesofágico (ERGE). Como abordaje inicial, si no existensíntomas de alarma, se puede dar una prueba terapéutica con inhibidor de bomba de pro-tones (IBP) por 2-4 semanas. Si hay disfagia o síntomas de alarma, se recomienda hacer unaendoscopia. La manometría de alta resolución es el mejor método para descartar trastornosmotores espásticos y acalasia. La pHmetría ayuda a demostrar exposición esofágica anormal alácido. El tratamiento debe ser dirigido al mecanismo fisiopatológico, y puede incluir IBP, neu-romoduladores y/o relajantes de músculo liso, intervención psicológica y/o terapia cognitiva,y ocasionalmente cirugía o terapia endoscópica. ABSTRACT Introduction: Non-cardiac chest pain is defined as a clinical syndrome characterized by retros-ternal pain similar to that of angina pectoris, but of non-cardiac origin and produced byesophageal, musculoskeletal, pulmonary, or psychiatric diseases.Aim: To present a consensus review based on evidence regarding the definition, epidemiology,pathophysiology, and diagnosis of non-cardiac chest pain, as well as the therapeutic options forthose patients. Methods: Three general coordinators carried out a literature review of all articles published inEnglish and Spanish on the theme and formulated 38 initial statements, dividing them into 3 maincategories: (i) definitions, epidemiology, and pathophysiology; (ii) diagnosis, and (iii) treatment.The statements underwent 3 rounds of voting, utilizing the Delphi system. The final statementswere those that reached > 75% agreement, and they were rated utilizing the GRADE system.Results and conclusions: The final consensus included 29 statements. All patients presentingwith chest pain should initially be evaluated by a cardiologist. The most common cause ofnon-cardiac chest pain is gastroesophageal reflux disease. If there are no alarm symptoms, the initial approach should be a therapeutic trial with a proton pump inhibitor for 2-4 weeks. Ifdysphagia or alarm symptoms are present, endoscopy is recommended. High-resolution mano-metry is the best method for ruling out spastic motor disorders and achalasia and pH monitoringaids in demonstrating abnormal esophageal acid exposure. Treatment should be directed at thepathophysiologic mechanism. It can include proton pump inhibitors, neuromodulators and/orsmooth muscle relaxants, psychologic intervention and/or cognitive therapy, and occasionallysurgery or endoscopic therapy

The Mexican consensus on non-cardiac chest pain

Introduction: Non-cardiac chest pain is defined as a clinical syndrome characterized by ret-rosternal pain similar to that of angina pectoris, but of non-cardiac origin and produced byesophageal, musculoskeletal, pulmonary, or psychiatric diseases. Aim: To present a consensus review based on evidence regarding the definition, epidemiology,pathophysiology, and diagnosis of non-cardiac chest pain, as well as the therapeutic options forthose patients. Methods Three general coordinators carried out a literature review of all articles published inEnglish and Spanish on the theme and formulated 38 initial statements, dividing them into 3 maincategories: 1) definitions, epidemiology, and pathophysiology, 2) diagnosis, and 3) treatment.The statements underwent 3 rounds of voting, utilizing the Delphi system. The final statementswere those that reached > 75% agreement, and they were rated utilizing the GRADE system. Results and conclusions The final consensus included 29 statements. All patients presentingwith chest pain should initially be evaluated by a cardiologist. The most common cause of non-cardiac chest pain is gastroesophageal reflux disease. If there are no alarm symptoms, the initialapproach should be a therapeutic trial with a proton pump inhibitor for 2-4 weeks. If dysphagiaor alarm symptoms are present, endoscopy is recommended. High-resolution manometry isthe best method for ruling out spastic motor disorders and achalasia and pH monitoring aidsin demonstrating abnormal esophageal acid exposure. Treatment should be directed at thepathophysiologic mechanism. It can include proton pump inhibitors, neuromodulators and/orsmooth muscle relaxants, psychologic intervention and/or cognitive therapy, and occasionallysurgery or endoscopic therapy

Search for Neutrinos in Super-Kamiokande Associated with the GW170817 Neutron-star Merger

We report the results of a neutrino search in Super-Kamiokande (SK) for coincident signals with the first detected gravitational wave (GW) produced by a binary neutron-star merger, GW170817, which was followed by a short gamma-ray burst, GRB170817A, and a kilonova/macronova. We searched for coincident neutrino events in the range from 3.5 MeV to ~100 PeV, in a time window ±500 s around the gravitational wave detection time, as well as during a 14-day period after the detection. No significant neutrino signal was observed for either time window. We calculated 90% confidence level upper limits on the neutrino fluence for GW170817. From the upward-going-muon events in the energy region above 1.6 GeV, the neutrino fluence limit is ${16.0}_{-0.6}^{+0.7}$ (${21.3}_{-0.8}^{+1.1}$) cm−2 for muon neutrinos (muon antineutrinos), with an error range of ±5° around the zenith angle of NGC4993, and the energy spectrum is under the assumption of an index of −2. The fluence limit for neutrino energies less than 100 MeV, for which the emission mechanism would be different than for higher-energy neutrinos, is also calculated. It is 6.6 × 107 cm−2 for anti-electron neutrinos under the assumption of a Fermi–Dirac spectrum with average energy of 20 MeV

Search for nucleon decay into charged antilepton plus meson in 0.316 megaton . years exposure of the Super-Kamiokande water Cherenkov detector

We have searched for proton decays into a charged antilepton (e+, μ+) plus a meson (η, ρ0, ω) and for neutron decays into a charged antilepton (e+, μ+) plus a meson (π−, ρ−) using Super-Kamiokande I-IV data, corresponding to 0.316  megaton⋅years of exposure. This measurement updates the previous published result by using 2.26 times more data and improved analysis methods. No significant evidence for nucleon decay is observed and lower limits on the partial lifetime of the nucleon are obtained. The limits range from 3×1031 to 1×1034  years at 90% confidence level, depending on the decay mode

Search for Boosted Dark Matter Interacting with Electrons in Super-Kamiokande

A search for boosted dark matter using 161.9 kt yr of Super-Kamiokande IV data is presented. We search for an excess of elastically scattered electrons above the atmospheric neutrino background, with a visible energy between 100 MeV and 1 TeV, pointing back to the Galactic center or the Sun. No such excess is observed. Limits on boosted dark matter event rates in multiple angular cones around the Galactic center and Sun are calculated. Limits are also calculated for a baseline model of boosted dark matter produced from cold dark matter annihilation or decay. This is the first experimental search for boosted dark matter from the Galactic center or the Sun interacting in a terrestrial detector

Reduced sympathetic stimulus and angiotensin 1-7 are related to diastolic dysfunction in spinal cord-injured subjects

CAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIOR - CAPESFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO ETECNOLOGICOChronic spinal cord injury (SCI) is often associated with reductions in left ventricular (LV) diastolic function. Impairments in sympathetic activity and activation of the renin-angiotensin system are reported in SCI individuals and may hypothetically be341523232328CAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIOR - CAPESFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO ETECNOLOGICOCAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIOR - CAPESFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO ETECNOLOGICOsem informaçãosem informaçãosem informaçã

A sweetpotato gene index established by de novo assembly of pyrosequencing and Sanger sequences and mining for gene-based microsatellite markers

Sweetpotato (Ipomoea batatas (L.) Lam.), a hexaploid outcrossing crop, is an important staple and food security crop in developing countries in Africa and Asia. The availability of genomic resources for sweetpotato is in striking contrast to its importance for human nutrition. Previously existing sequence data were restricted to around 22,000 expressed sequence tag (EST) sequences and ~ 1,500 GenBank sequences. We have used 454 pyrosequencing to augment the available gene sequence information to enhance functional genomics and marker design for this plant species

Prevalence and clinical outcomes of dystrophin-associated dilated cardiomyopathy without severe skeletal myopathy

Aims: Dilated cardiomyopathy (DCM) associated with dystrophin gene (DMD) mutations in individuals with mild or absent skeletal myopathy is often indistinguishable from other DCM forms. We sought to describe the phenotype and prognosis of DMD associated DCM in DMD mutation carriers without severe skeletal myopathy. Methods and results: At 26 European centres, we retrospectively collected clinical characteristics and outcomes of 223 DMD mutation carriers (83% male, 33 ± 15 years). A total of 112 individuals (52%) had DCM at first evaluation [n = 85; left ventricular ejection fraction (LVEF) 34 ± 11.2%] or developed DCM (n = 27; LVEF 41.3 ± 7.5%) after a median follow-up of 96 months (interquartile range 5–311 months). DCM penetrance was 45% in carriers older than 40 years. DCM appeared earlier in males and was independent of the type of mutation, presence of skeletal myopathy, or elevated serum creatine kinase levels. Major adverse cardiac events (MACE) occurred in 22% individuals with DCM, 18% developed end-stage heart failure and 9% sudden cardiac death or equivalent. Skeletal myopathy was not associated with survival free of MACE in patients with DCM. Decreased LVEF and increased left ventricular end-diastolic diameter at baseline were associated with MACE. Individuals without DCM had favourable prognosis without MACE or death during follow-up. Conclusions: DMD-associated DCM without severe skeletal myopathy is characterized by incomplete penetrance but high risk of MACE, including progression to end-stage heart failure and ventricular arrhythmias. DCM onset is the major determinant of prognosis with similar survival regardless of the presence of skeletal myopathy