Apremios sobre los posgrados

La vida universitaria integra un funcionamiento un tanto paradójico. Por una parte acentúa la fragmentación de las prácticas (docencia, investigación individual y gestión, teóricos y prácticos, asignatura, áreas, disciplinas) y por la otra, depende de la articulación de niveles (años de cursado, correlatividades de contenidos, grado y posgrado). Esta tensión entre fragmentación y articulación suele no resolverse adecuadamente y tiene como efecto principal la necesidad de bruscas adaptaciones de los actores institucionales (principalmente estudiantes, docentes, investigadores) ante las nuevas situaciones planteadas. Para reflexionar sobre el posgrado deberíamos partir de este marco, ya que en los últimos años el crecimiento exponencial de los posgrados en comunicación y cultura nos advierte que los riesgos mencionados no fueron salvados.Facultad de Periodismo y Comunicación Socia

Apremios sobre los posgrados

La vida universitaria integra un funcionamiento un tanto paradójico. Por una parte acentúa la fragmentación de las prácticas (docencia, investigación individual y gestión, teóricos y prácticos, asignatura, áreas, disciplinas) y por la otra, depende de la articulación de niveles (años de cursado, correlatividades de contenidos, grado y posgrado). Esta tensión entre fragmentación y articulación suele no resolverse adecuadamente y tiene como efecto principal la necesidad de bruscas adaptaciones de los actores institucionales (principalmente estudiantes, docentes, investigadores) ante las nuevas situaciones planteadas. Para reflexionar sobre el posgrado deberíamos partir de este marco, ya que en los últimos años el crecimiento exponencial de los posgrados en comunicación y cultura nos advierte que los riesgos mencionados no fueron salvados.Facultad de Periodismo y Comunicación Socia

El discurso del periodismo deportivo: entre las filosofías de la vida y la guerra por otros medios

No presenta resumen

Smad2 and Smad6 as predictors of overall survival in oral squamous cell carcinoma patients

Background: To test if the expression of Smad1-8 mRNAs were predictive of survival in patients with oral squamous cell carcinoma (SCC). Patients and Methods: We analyzed, prospectively, the expression of Smad1-8, by means of Ribonuclease Protection Assay in 48 primary, operable, oral SCC. In addition, 21 larynx, 10 oropharynx and 4 hypopharynx SCC and 65 matched adjacent mucosa, available for study, were also included. For survival analysis, patients were categorized as positive or negative for each Smad, according to median mRNA expression. We also performed real-time quantitative PCR (QRTPCR) to asses the pattern of TGF beta 1, TGF beta 2, TGF beta 3 in oral SCC. Results: Our results showed that Smad2 and Smad6 mRNA expression were both associated with survival in Oral SCC patients. Cox Multivariate analysis revealed that Smad6 positivity and Smad2 negativity were both predictive of good prognosis for oral SCC patients, independent of lymph nodal status (P = 0.003 and P = 0.029, respectively). In addition, simultaneously Smad2(-) and Smad6(+) oral SCC group of patients did not reach median overall survival (mOS) whereas the mOS of Smad2(+)/Smad6(-) subgroup was 11.6 months (P = 0.004, univariate analysis). Regarding to TGF beta isoforms, we found that Smad2 mRNA and TGF beta 1 mRNA were inversely correlated (p = 0.05, R = -0.33), and that seven of the eight TGF beta 1(+) patients were Smad2(-). In larynx SCC, Smad7(-) patients did not reach mOS whereas mOS of Smad7(+) patients were only 7.0 months (P = 0.04). No other correlations were found among Smad expression, clinico-pathological characteristics and survival in oral, larynx, hypopharynx, oropharynx or the entire head and neck SCC population. Conclusion: Smad6 together with Smad2 may be prognostic factors, independent of nodal status in oral SCC after curative resection. The underlying mechanism which involves aberrant TGF beta signaling should be better clarified in the future.FAPESP[02/01738-9]CNP

Cognitive Impairment Centralized Case Registry in Argentina (ReDeCAr) based on Epidemiological Surveillance Model

Se propone el desarrollo de un Registro centralizado de casos de Deterioro Cognitivo en Argentina (ReDeCAr) basado en el modelo de vigilancia epidemiológica. Se llevará a cabo un estudio de tipo observacional prospectivo en distintos centros y hospitales del sistema de salud de todo el país. Para la recolección de datos se utilizará un software de alcance nacional que incluya los sistemas de vigilancia epidemiológica en un mismo formato, estableciendo una red de vigilancia. Dicha red estará conectada a internet, sitio web del Ministerio de Salud de la Nación (www.msal.gov.ar). Estos datos serán útiles para describir patrones de ocurrencia por subtipos, identificar sus principales características clínicas y generar hipótesis para nuevos proyectos de investigación clínica. Se establecerá una unidad de referencia común para una problemática que requiere atención social y sanitaria multidisciplinaria. Esto permitirá inferir la importancia local de esta patología, para lo cual es necesario disponer de datos poblacionales que generen adecuadas políticas de salud.This paper presents a proposal for the development of a Cognitive Impairment Centralized Case Registry in Argentina (ReDeCAr) based on Epidemiological Surveillance Model. We will conduct an observational prospective study in different healthcare centers and hospitals around the country. For data collection, we will use nationwide software including epidemiological surveillance systems with the same format that together form an Internet-based surveillance network that will appear on the Ministry of Health website (www.msal.gov.ar). These data will be useful to describe occurrence patterns of different subtypes, to identify the main clinical characteristics of patients and to develop new clinical research projects. We will determine a common reference unit for a health problem that requires social attention and a multidisciplinary approach. This will show the local impact of these pathologies and it will provide population-based data necessary to develop sound health policies.Fil: Melcon, Carlos Mario. Ministerio de Salud de la Nación; ArgentinaFil: Bartoloni, Leonardo Carlos. Ministerio de Salud de la Nación; ArgentinaFil: Katz, Marcelo Esteban. Ministerio de Salud de la Nación; ArgentinaFil: Del Mónaco, Rodrigo. Ministerio de Salud de la Nación; ArgentinaFil: Mangone, Carlos A.. Gobierno de la Ciudad Autónoma de Buenos Aires. Ministerio de Salud; ArgentinaFil: Melcon, Mario Osacar. Fundación Para la Investigación En Neuroepidemiología; ArgentinaFil: Allegri, Ricardo Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Gobierno de la Ciudad Autónoma de Buenos Aires. Ministerio de Salud; Argentin

Transethnic meta-analysis of rare coding variants in PLCG2, ABI3, and TREM2 supports their general contribution to Alzheimer’s disease

Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer’s disease (AD) in Caucasians. Frequencies and AD-associated effects of variants differ across ethnicities. To start filling the gap on AD genetics in South America and assess the impact of these variants across ethnicity, we studied these variants in Argentinian population in association with ancestry. TREM2 (rs143332484 and rs75932628), PLCG2 (rs72824905), and ABI3 (rs616338) were genotyped in 419 AD cases and 486 controls. Meta-analysis with European population was performed. Ancestry was estimated from genome-wide genotyping results. All variants show similar frequencies and odds ratios to those previously reported. Their association with AD reach statistical significance by meta-analysis. Although the Argentinian population is an admixture, variant carriers presented mainly Caucasian ancestry. Rare coding variants in TREM2, PLCG2, and ABI3 also modulate susceptibility to AD in populations from Argentina, and they may have a European heritage.International Society for Neurochemistry (ISN) and Alexander von Humboldt Foundation (to M.C.D.); Agencia Nacional de Promoción Científica y Tecnológica (PBIT/09 2013, PICT2015-0285 and PICT-2016-4647 to L.M.; PICT-2014-1537 to M.C.D.

Alzheimer's disease: Clinical practice guideline

El Grupo de Trabajo de Neurología de la Conducta y Neurociencias Cognitivas de la Sociedad Neurológica Argentina publicó en 2006 la primera Guía de práctica clínica sobre la enfermedad de Alzheimer para su aplicación en nuestro medio y, eventualmente, en el resto de los países hispanoparlantes del Cono Sur. La Guía que hoy publicamos, mediante la revisión y actualización del estado actual del conocimiento sobre la enfermedad de Alzheimer y su manejo clínico y neurológico, provee a los profesionales los estándares surgidos de la medicina basada en la evidencia para una adecuada implementación de las conductas diagnósticas y terapéuticas a su alcance en nuestro medio.In 2006, the Argentine Neurological Society Research Group on Behavioral Neurology and Cognitive Neurosciences published the first Clinical Practice Guideline on Alzheimer's Disease to be consulted in Argentina and eventually in other countries in Latin America. The present Guideline is a review of the state of the art concerning the 2010 knowledge on the management of this disease. It provides physicians with the usual standards provided by evidence based medicine in order to reach the most adequate diagnostic and therapeutic measures at hand in our countries.Fil: Allegri, Ricardo Francisco. Sociedad Neurológica Argentina; Argentina. Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia. Instituto de Neurociencias - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Neurociencias; ArgentinaFil: Arizaga, Raúl Luciano. Sociedad Neurológica Argentina; ArgentinaFil: Bavec, Claudia V.. Sociedad Neurológica Argentina; ArgentinaFil: Colli, Liliana P.. Sociedad Neurológica Argentina; ArgentinaFil: Demey, Ignacio. Sociedad Neurológica Argentina; ArgentinaFil: Fernández, María C.. Sociedad Neurológica Argentina; ArgentinaFil: Frontera, Silvina A.. Sociedad Neurológica Argentina; ArgentinaFil: Garau, María L.. Sociedad Neurológica Argentina; ArgentinaFil: Jiménez, Julio J.. Sociedad Neurológica Argentina; ArgentinaFil: Golimstok, Angel. Sociedad Neurológica Argentina; ArgentinaFil: Kremer, Janus. Sociedad Neurológica Argentina; ArgentinaFil: Labos, Edith. Sociedad Neurológica Argentina; ArgentinaFil: Mangone, Carlos Antonio. Sociedad Neurológica Argentina; ArgentinaFil: Ollari, Juan A.. Sociedad Neurológica Argentina; ArgentinaFil: Rojas, Zenón Galeno. Centro de Educación Médica e Investigaciones Clínicas "Norberto Quirno"; Argentina. Sociedad Neurológica Argentina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Salmini, Omar. Sociedad Neurológica Argentina; ArgentinaFil: Ure, Jorge A.. Sociedad Neurológica Argentina; ArgentinaFil: Zuin, Daniel R.. Sociedad Neurológica Argentina; Argentin

PTPA variants and impaired PP2A activity in early-onset parkinsonism with intellectual disability

The protein phosphatase 2A complex (PP2A), the major Ser/Thr phosphatase in the brain, is involved in a number of signalling pathways and functions, including the regulation of crucial proteins for neurodegeneration, such as alpha-synuclein, tau and LRRK2. Here, we report the identification of variants in the PTPA/PPP2R4 gene, encoding a major PP2A activator, in two families with early-onset parkinsonism and intellectual disability. We carried out clinical studies and genetic analyses, including genome-wide linkage analysis, whole-exome sequencing, and Sanger sequencing of candidate variants. We next performed functional studies on the disease-associated variants in cultured cells and knock-down of ptpa in Drosophila melanogaster. We first identified a homozygous PTPA variant, c.893T&gt;G (p.Met298Arg), in patients from a South African family with early-onset parkinsonism and intellectual disability. Screening of a large series of additional families yielded a second homozygous variant, c.512C&gt;A (p.Ala171Asp), in a Libyan family with a similar phenotype. Both variants co-segregate with disease in the respective families. The affected subjects display juvenile-onset parkinsonism and intellectual disability. The motor symptoms were responsive to treatment with levodopa and deep brain stimulation of the subthalamic nucleus. In overexpression studies, both the PTPA p.Ala171Asp and p.Met298Arg variants were associated with decreased PTPA RNA stability and decreased PTPA protein levels; the p.Ala171Asp variant additionally displayed decreased PTPA protein stability. Crucially, expression of both variants was associated with decreased PP2A complex levels and impaired PP2A phosphatase activation. PTPA orthologue knock-down in Drosophila neurons induced a significant impairment of locomotion in the climbing test. This defect was age-dependent and fully reversed by L-DOPA treatment. We conclude that bi-allelic missense PTPA variants associated with impaired activation of the PP2A phosphatase cause autosomal recessive early-onset parkinsonism with intellectual disability. Our findings might also provide new insights for understanding the role of the PP2A complex in the pathogenesis of more common forms of neurodegeneration.</p