What's That Object? Learning Astronomical Concepts Through The Use Of The Aladin Program And Manipulation Of Astronomical Images

Various studies have noted current shortcomings in the teaching and learning of science in schools, and the results of large-scale tests show that despite heavy investment in education, Brazilians' understanding of science test scores typically fall short of what could be if students had a consistent, high-quality basic education. This article summarizes the teaching plan and systematic study results for an activity titled "What’s That Object?" implemented in the city of Salvador, Bahia state, Brazil, in 2015. Astronomical concepts were taught, and the Aladin software was used in the lessons, which included two computerized memory games produced for this activity.We believe that the results lend strong support to the notion that astronomy education can be improved and motivates educators to teach astronomical concepts at the elementary school level

Mioclonías asociadas al tratamiento con ciprofloxacino

Las quinolonas son un grupo de antibióticos que actúan inhibiendo la síntesis bacteriana de DNA al ejercer su efecto sobre la topoisomerasa II, así como sobre la topoisomerasa IV. Son fármacos de gran espectro de actividad que se utilizan en gran cantidad de infecciones, como las de tracto urinario, piel, hueso y aparato respiratorio. Los efectos adversos más frecuentes de las quinolo- nas son los de tipo gastrointestinal, que suelen ser leves. Además, son importantes los efectos sobre el sistema nervioso como mareos, insomnio, somnolencia, confusión, temblores, etc. Son efectos que aparecen de forma precoz y desaparecen al suspender el tratamient

The Neuroprotective Action of Amidated-Kyotorphin on Amyloid β Peptide-Induced Alzheimer’s Disease Pathophysiology

Kyotorphin (KTP, l-tyrosyl-l-arginine) is an endogenous dipeptide initially described to have analgesic properties. Recently, KTP was suggested to be an endogenous neuroprotective agent, namely for Alzheimer’s disease (AD). In fact, KTP levels were shown to be decreased in the cerebrospinal fluid of patients with AD, and recent data showed that intracerebroventricular (i.c.v.) injection of KTP ameliorates memory impairments in a sporadic rat model of AD. However, this administration route is far from being a suitable therapeutic strategy. Here, we evaluated if the blood-brain permeant KTP-derivative, KTP-NH2, when systemically administered, would be effective in preventing memory deficits in a sporadic AD animal model and if so, which would be the synaptic correlates of that action. The sporadic AD model was induced in male Wistar rats through i.c.v. injection of amyloid β peptide (Aβ). Animals were treated for 20 days with KTP-NH2 (32.3 mg/kg, intraperitoneally (i.p.), starting at day 3 after Aβ administration) before memory testing (Novel object recognition (NOR) and Y-maze (YM) tests). Animals were then sacrificed, and markers for gliosis were assessed by immunohistochemistry and Western blot analysis. Synaptic correlates were assessed by evaluating theta-burst induced long term potentiation (LTP) of field excitatory synaptic potentials (fEPSPs) recorded from hippocampal slices and cortical spine density analysis. In the absence of KTP-NH2 treatment, Aβ-injected rats had clear memory deficits, as assessed through NOR or YM tests. Importantly, these memory deficits were absent in Aβ-injected rats that had been treated with KTP-NH2, which scored in memory tests as control (sham i.c.v. injected) rats. No signs of gliosis could be detected at the end of the treatment in any group of animals. LTP magnitude was significantly impaired in hippocampal slices that had been incubated with Aβ oligomers (200 nM) in the absence of KTP-NH2. Co-incubation with KTP-NH2 (50 nM) rescued LTP toward control values. Similarly, Aβ caused a significant decrease in spine density in cortical neuronal cultures, and this was prevented by co-incubation with KTP-NH2 (50 nM). In conclusion, the present data demonstrate that i.p. KTP-NH2 treatment counteracts Aβ-induced memory impairments in an AD sporadic model, possibly through the rescuing of synaptic plasticity mechanisms.publishersversionpublishe

Asociación entre el síndrome metabólico y los niveles de transaminasas

Introducción: En la patología del síndrome metabólico, de acuerdo con distintas investigaciones y la práctica clínica se han visto manifestaciones de daño hepático. Objetivo: Estimar la prevalencia de transaminasas elevadas (alanina aminotransaminasa y aspartato aminotransaminasa) y determinar su asociación con síndrome metabólico. Métodos: Estudio transversal con procedimientos analíticos. Análisis secundario de los datos generados por el registro electrónico en salud de un policlínico ocupacional. La variable principal fue el diagnóstico del síndrome metabólico. Para definir aspartato aminotransaminasa elevada se consideraron valores > 30 U/L en mujeres y valores > 36 U/L en hombres. Para alanina aminotransaminasa, se consideraron valores > 30 U/L en mujeres y valores > 40 U/L en hombres. Resultados: La prevalencia de síndrome metabólico fue de 21,82 %, de aspartato aminotransaminasa elevada fue del 10,30 % y alanina aminotransaminasa elevada del 16,67 %. En la regresión múltiple, se ajustó por las covariables confusoras sexo, edad, ocupación, índice de masa corporal, fumar, alcohol y actividad física. Se observó que los pacientes con aspartato aminotransaminasa elevada tenían 128 % mayor frecuencia de síndrome metabólico, respecto a quienes no presentaban valores elevados (razón prevalencia= 2,28; IC95 %: 1,64 – 3,17; p< 0,001). Se encontró que los pacientes con alanina aminotransaminasa elevada tenían 148 % mayor frecuencia de presentar síndrome metabólico respecto a quienes no presentaban valores elevados (razón prevalencia= 2,48; IC95 %: 1,77 – 3,47; p< 0,001). Conclusiones: Existe asociación entre las transaminasas hepáticas elevadas y la presencia de síndrome metabólico.Campus Lima Nort

Violencia política y conflictos sociales en América Latina

La violencia socio-económica como categoría de estudio en las ciencias sociales y humanas, ha venido adquiriendo creciente relevancia en América Latina. Los problemas y variables metodológicas asociadas a su investigación han sido abordados con mayor profundidad desde la sociología, el Derecho, la Ciencia política y la Psicología Social. Es por esto, que esta publicación se propone abordar la violencia socio-económica como una categoría de análisis e investigación interdisciplinaria, posibilitando la reflexión académica en torno a las dinámicas de construcción del poder, la institucionalidad y los movimientos sociales en América Latina.Introducción; Parte I. Violencia, derechos humanos y criminalidad. Conflicto y violencias en Colombia / Roberto González Arana, Ivonne Molinares Guerrero; Derechos humanos y seguridad democrática en Colombia: ¿un equilibrio posible? / César Barreira; Conflictividad, violencia y control social: saberes latinoamericanos contemporáneos / José Vicente Tavares-dos-Santos; Pensar la justicia de adolescentes desde el campo jurídico / Nilia Viscardi, Marcia Barbero; Parte ii. Conflictos: armados, étnicos, territoriales y por los recursos naturales. Aproximaciones teórico-conceptuales en torno al conflicto armado colombiano / Luis Fernando Trejos Rosero; El conflicto mapuche y el estado de Chile: una reflexión sobre la violencia y la imagen de Chile en el bicentenario / Loreto Correa V.; Entre la violencia política y social. Una revisión a la inmigración africana subsahariana occidental en Buenos Aires (1990-2010) / Mary Luz Estupiñán Serrano; Producción de nuevas espacialidades y cambios de autoridad. Interacción globalización-conflicto armado-grupos étnicos / Clara Inés Aramburo Siegert; Los recursos mineros y la protesta ciudadana en la Argentina de la última década / Orietta Favaro, Graciela Iuorno; Performances do crime: componentes dramáticos e teatrais dos grandes roubos no Brasil / Jania Perla Diógenes de Aquino

A genome-wide association study follow-up suggests a possible role for PPARG in systemic sclerosis susceptibility

Introduction: A recent genome-wide association study (GWAS) comprising a French cohort of systemic sclerosis (SSc) reported several non-HLA single-nucleotide polymorphisms (SNPs) showing a nominal association in the discovery phase. We aimed to identify previously overlooked susceptibility variants by using a follow-up strategy.&lt;p&gt;&lt;/p&gt; Methods: Sixty-six non-HLA SNPs showing a P value &#60;10-4 in the discovery phase of the French SSc GWAS were analyzed in the first step of this study, performing a meta-analysis that combined data from the two published SSc GWASs. A total of 2,921 SSc patients and 6,963 healthy controls were included in this first phase. Two SNPs, PPARG rs310746 and CHRNA9 rs6832151, were selected for genotyping in the replication cohort (1,068 SSc patients and 6,762 healthy controls) based on the results of the first step. Genotyping was performed by using TaqMan SNP genotyping assays. Results: We observed nominal associations for both PPARG rs310746 (PMH = 1.90 × 10-6, OR, 1.28) and CHRNA9 rs6832151 (PMH = 4.30 × 10-6, OR, 1.17) genetic variants with SSc in the first step of our study. In the replication phase, we observed a trend of association for PPARG rs310746 (P value = 0.066; OR, 1.17). The combined overall Mantel-Haenszel meta-analysis of all the cohorts included in the present study revealed that PPARG rs310746 remained associated with SSc with a nominal non-genome-wide significant P value (PMH = 5.00 × 10-7; OR, 1.25). No evidence of association was observed for CHRNA9 rs6832151 either in the replication phase or in the overall pooled analysis.&lt;p&gt;&lt;/p&gt; Conclusion: Our results suggest a role of PPARG gene in the development of SSc

Measurement of the cross-section and charge asymmetry of WW bosons produced in proton-proton collisions at s=8\sqrt{s}=8 TeV with the ATLAS detector

This paper presents measurements of the $W^+ \rightarrow \mu^+\nu$ and $W^- \rightarrow \mu^-\nu$ cross-sections and the associated charge asymmetry as a function of the absolute pseudorapidity of the decay muon. The data were collected in proton--proton collisions at a centre-of-mass energy of 8 TeV with the ATLAS experiment at the LHC and correspond to a total integrated luminosity of 20.2~\mbox{fb^{-1}}. The precision of the cross-section measurements varies between 0.8% to 1.5% as a function of the pseudorapidity, excluding the 1.9% uncertainty on the integrated luminosity. The charge asymmetry is measured with an uncertainty between 0.002 and 0.003. The results are compared with predictions based on next-to-next-to-leading-order calculations with various parton distribution functions and have the sensitivity to discriminate between them.Comment: 38 pages in total, author list starting page 22, 5 figures, 4 tables, submitted to EPJC. All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/STDM-2017-13

Search for chargino-neutralino production with mass splittings near the electroweak scale in three-lepton final states in √s=13 TeV pp collisions with the ATLAS detector

A search for supersymmetry through the pair production of electroweakinos with mass splittings near the electroweak scale and decaying via on-shell W and Z bosons is presented for a three-lepton final state. The analyzed proton-proton collision data taken at a center-of-mass energy of √s=13  TeV were collected between 2015 and 2018 by the ATLAS experiment at the Large Hadron Collider, corresponding to an integrated luminosity of 139  fb−1. A search, emulating the recursive jigsaw reconstruction technique with easily reproducible laboratory-frame variables, is performed. The two excesses observed in the 2015–2016 data recursive jigsaw analysis in the low-mass three-lepton phase space are reproduced. Results with the full data set are in agreement with the Standard Model expectations. They are interpreted to set exclusion limits at the 95% confidence level on simplified models of chargino-neutralino pair production for masses up to 345 GeV

Real-Time PCR in HIV/Trypanosoma cruzi Coinfection with and without Chagas Disease Reactivation: Association with HIV Viral Load and CD4+ Level

Chagas disease is endemic in Latin America and is caused by the flagellate protozoan T. cruzi. The acute phase is asymptomatic in the majority of the cases and rarely causes inflammation of the heart or the central nervous system. Most infected patients progress to a chronic phase, characterized by cardiac or digestive involvement when not asymptomatic. However, when patients are also exposed to an immunosuppressant (such as chemotherapy), neoplasia, or other infections such as HIV, T. cruzi infection may develop into a severe disease (Chagas disease reactivation) involving the heart and central nervous system. The current microscopic methods for diagnosing Chagas disease reactivation are not sensitive enough to prevent the high rate of death observed in these cases. Therefore, we propose a quantitative method to monitor blood levels of the parasite, which will allow therapy to be administered as early as possible, even if the patient has not yet presented symptoms

Sustained proliferation in cancer: mechanisms and novel therapeutic targets

Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression