TRABAJO PEDAGOGICO CON LOS PADRES DE FAMILIA

Al final del periodo respectivo, el rector y cada docente director de sede desarrollan concomitantemente con la entrega de boletines actividades pedagógicas de formación democrática, legislación del menor, desarrollo de valores personales y familiares, talleres de los proyectos transversales incluyendo la "Escuela de Familia" y actualización de la información institucional sobre los procesos académicos, administrativos y financieros. Se observa a continuación a los padres de familia y acudientes participantes en cada una de las sedes, con el rector y los docentes en esta labor.

Sede Central Atanasio Girardot. Padres de familia, rector y docente Miriam Saldarriaga.

Padres Sede San Agustín y el Docente Juan C. Zapata S.

Padres de familia Sede Antonio Ricaurte y las docentes Aura M. Sánchez y Mónica Valencia

Padres Sede Juan M Céspedes y Docente Jenny P. Arboleda

Padres Sede Pedro Pablo de la Cruz y Docente Xiomara Rodriguez G.

Padres de la Sede María Palacios y Docente Alba L. Carmona R.

Padres Sede José C. Mutis y la Docente Claudia L. Ochoa C.

Padres Sede Guillermo Valencia y Docente Paola A. Giraldo O.

Nuevo segmento genómico relacionado con la aparición de la enfermedad de Alzheimer

APOE-TOMM40 in the Pharmacogenomics of Dementia

Abstract

Polymorphic variants present in the APOE-TOMM40 region (19q13.2) are implicated in Alzheimer’s disease (AD) and have been shown to modify disease risk, age at onset of symptoms, and the therapeutic response to conventional drugs. We have investigated the structure of the APOE-TOMM40 region and the influence of APOE and TOMM40 poly T variants (rs10524523) in the therapeutic response to a multifactorial treatment in 920 Spanish patients with AD. The frequencies of TOMM40 poly T genotypes were: 18.37% S/S, 7.83% S/L, 38.80% S/VL, 1.52% L/L, 7.17% L/VL, and 26.31% VL/VL. The most frequent APOE-TOMM40 associations were as follows: 82% APOE-3/3 with S/S, 63% with S/VL, and 40% with VL/VL; 90% APOE-3/4 with S/L, 57% with L/VL, and 43% with VL/VL; and 100% APOE-4/4 with L/L. Globally, the response rate was about 59%, with no difference between females and males. APOE-4 carriers were found to be the worst responders (45-56%) whereas APOE-3/3 carriers were the best responders (70%) for a transient period of cognitive improvement (<12 a="" ad.="" among="" and="" apoe-tomm40="" best="" by="" carriers="" conventional="" exert="" followed="" genotype="" harboring="" in="" influence="" l="" m="" on="" p="" patients="" poly="" powerful="" responders="" response="" s="" specific="" t="" the="" therapeutic="" therefore="" those="" to="" tomm40="" treatments="" variants="" vl="" were="" worst="">

Keywords

Alzheimer’s disease; APOE; Multifactorial treatment; Pharmacogenomics; Therapeutic response rate; TOMM40

Abbreviations

A2BP1: Ataxin-2 Binding Protein 1; ABAT: 4-aminobutyrate aminotransferase; ABCA7: ATP-binding cassette, sub-family A (ABC1), member 7; ABCB1: ATP-binding cassette, sub-family B (MDR/TAP), member 1; ABCs: ATPbinding cassette family; ABO: ABO blood group (transferase A, alpha 1-3-N-acetylgalactosaminyltransferase; transferase B, alpha 1-3-galactosyltransferase); ACE: Angiotensin I Converting Enzyme; AD: Alzheimer’s Disease; AGT: Angiotensinogen; APOC1: Apolipoprotein C-I; APOC2: Apolipoprotein C-II; APOC4: Apolipoprotein C-IV; APOE: Apolipoprotein E; APOs: Apolipoproteins; APP: Amyloid beta (A4) Precursor Protein; BIN1: Bridging Integrator 1; CD2AP: CD2-associated protein; CDH2: Cadherin 2, type 1; CLU: Clusterin; CNVs: Copy Number Variations; CR1: Complement Component (3b/4b) Receptor 1; CRMP1: Collapsin Response Mediator Protein 1; CRP: C-reactive protein; CVD: Cardiovascular Disease; CYP2D6: Cytochrome P450, family 2, subfamily D, polypeptide 6; CYPs: Cytochrome P450 family; DMRT1: Doublesex and mab-3 related transcription factor 1; EO-FAD: Earlyonset Familial Alzheimer’s Disease; EPHA5: EPH receptor A5; EPHA6: EPH receptor A6; ERMP1: Endoplasmic Reticulum metallopeptidase 1; GWAS: Genome-wide Association Studies; HMGCR: 3-hydroxy- 3-methylglutaryl-CoA reductase; ILs: Interleukins; L: Long; LOAD: Late Onset Alzheimer’s Disease; MAPT: Microtubule-associated protein tau; MS4A4E: Membrane-spanning 4-domains, subfamily A, member 4E ; MS4A6A: Membrane-spanning 4-domains, subfamily A, member 6A; MTHFR: Methylenetetrahydrofolate Reductase (NAD(P) H); NATs: N-acetyltransferase family; NFT: Neurofibrillary Tangles; NOS: Nitric Oxide Synthase; PICALM: Phosphatidylinositol binding clathrin assembly protein; PRNP: Prion protein; PSEN1: Presenilin 1; PSEN2: Presenilin 2; S: Short; SLCs: Solute Carrier Family; SNPs: Single-nucleotide Polymorphisms; TOMM40: Translocase of Outer Mitochondrial Membrane 40 homolog (yeast); UGTs: UDP glucuronosyltransferase family; VL: Very Long; VLDLR: Very Low Density Lipoprotein Receptor

Un estudio observa efectos positivos de la fibra de Plantago ovata en pacientes con enfermedad de Parkinson

A randomised clinical trial to evaluate the effects of Plantago ovata husk in Parkinson patients: changes in levodopa pharmacokinetics and biochemical parameters

Abstract

Background

Plantago ovata husk therapy could be used in patients with Parkinson disease to reduce the symptoms of gastrointestinal disorders, but it is important to know whether this compound modifies levodopa pharmacokinetics. The maintenance of constant plasma concentrations of levodopa abolishes the clinical fluctuations in parkinsonian patients. The aim of this randomised clinical trial was to establish the influence of the fiber Plantago ovata husk in the pharmacokinetics of levodopa when administered to Parkinson patients well controlled by their oral medication.

Methods

To evaluate the effects of this fiber on several biochemical parameters. 18 volunteers participated in the study and received alternatively two treatments (Plantago ovata husk or placebo) with their usual levodopa/carbidopa oral dose. On days 0 (initial situation), 14 and 35 of the study, blood samples were taken to assess levodopa pharmacokinetics and to determine biochemical parameters.

Results

Levodopa Cmax was very similar in the initial situation (603.2 ng/ml) and after placebo administration (612.0 ng/ml), being slightly lower (547.8 ng/ml) when Plantago ovata husk was given. AUC was very similar in the three groups: initial situation.- 62.87 μg.min/ml, fiber treatment.- 64.47 μg.min/ml and placebo treatment.- 65.10 μg.min/ml. Fiber reduced significantly the number of peaks observed in the levodopa concentrations, maintaining concentrations more stable. No significant differences were found in total cholesterol, LDL-cholesterol and triglycerides with the administration of Plantago ovata husk.

Conclusions

Plantago ovata husk administration caused a smoothing and homogenization of levodopa absorption, providing more stable concentrations and final higher levels, resulting in a great benefit for patients.

Identifican mutaciones genéticas con un papel clave en la encefalopatía epiléptica

De novo mutations in synaptic transmission genes including DNM1 cause epileptic encephalopathies.

Abstract

Emerging evidence indicates that epileptic encephalopathies are genetically highly heterogeneous, underscoring the need for large cohorts of well-characterized individuals to further define the genetic landscape. Through a collaboration between two consortia (EuroEPINOMICS and Epi4K/EPGP), we analyzed exome-sequencing data of 356 trios with the "classical" epileptic encephalopathies, infantile spasms and Lennox Gastaut syndrome, including 264 trios previously analyzed by the Epi4K/EPGP consortium. In this expanded cohort, we find 429 de novo mutations, including de novo mutations in DNM1 in five individuals and de novo mutations in GABBR2, FASN, and RYR3 in two individuals each. Unlike previous studies, this cohort is sufficiently large to show a significant excess of de novo mutations in epileptic encephalopathy probands compared to the general population using a likelihood analysis (p = 8.2 × 10(-4)), supporting a prominent role for de novo mutations in epileptic encephalopathies. We bring statistical evidence that mutations in DNM1 cause epileptic encephalopathy, find suggestive evidence for a role of three additional genes, and show that at least 12% of analyzed individuals have an identifiable causal de novo mutation. Strikingly, 75% of mutations in these probands are predicted to disrupt a protein involved in regulating synaptic transmission, and there is a significant enrichment of de novo mutations in genes in this pathway in the entire cohort as well. These findings emphasize an important role for synaptic dysregulation in epileptic encephalopathies, above and beyond that caused by ion channel dysfunction. 

Mujeres de mediana edad con neurosis y ansiedad, en mayor riesgo de desarrollar enfermedad de Alzheimer

Midlife personality and risk of Alzheimer disease and distress

ABSTRACT

Objective: To study the association between midlife neuroticism and extraversion and development of late-life dementia and long-standing distress in a sample of women followed for 38 years.

Methods: A population-based sample of 800 women, aged 38 to 54 years, was examined in 1968, with subsequent examinations in 1974, 1980, 1992, 2000, and 2005. Neuroticism and extraversion were assessed using the Eysenck Personality Inventory at baseline. Distress was measured according to a standardized question at each study wave. Dementia was diagnosed according to DSM-III-R criteria based on information from neuropsychiatric examinations, informant interviews, hospital records, and registry data.

Results: During the 38-year follow-up, 153 women developed dementia; Alzheimer disease (AD) dementia was diagnosed in 104 of these. A higher degree of neuroticism in midlife was associated with increased risk of AD dementia and long-standing distress over 38 years. The association between neuroticism and AD dementia diminished after adjusting for long-standing distress. Extraversion was associated with a lower degree of long-standing distress, but had no impact on AD dementia. When the 2 personality dimensions were combined, high neuroticism/low extraversion showed the highest risk of AD dementia.

Conclusions: Our study suggests that midlife neuroticism is associated with increased risk of AD dementia, and that distress mediates this association. The results have clinical implications because a group of women at risk of AD dementia is identified.

PROYECTO PALABRARIO: UN EJE MOTIVADOR DEL TRABAJO EN EQUIPO

EXPERIENCIA SIGNIFICATIVA DE LAS SEDES: GUILLERMO VALENCIA Y SAN AGUSTIN

Los docentes PAOLA ANDREA GIRALDO Y JUAN CARLOS ZAPATA, de las sedes antes mencionadas, creemos firmemente que el trabajo en equipo da mas frutos y aun mas significativos que el trabajo individual, por esto hemos buscado espacios como celebraciones especiales en los que integramos las dos sedes, además de la integración de los padres de familia.

Celebración día de los niños

Optimizando el uso de la sala de lectura donada por la fundación carvajal, fundación corona y los patrocinadores del proyecto "Palabrario" organizamos actividades de lecto - escritura, caligrafía y juegos didácticos que llevan al estudiante a interesarse mas por la lectura y producir sus propios textos.

También nos interesa despertar en estos niños sus procesos motores para que se reflejen en su expresión corporal y manejar la timidez que es tan marcada en ellos.

En el tiempo en que hemos utilizado estos espacios los niños de las dos sedes han establecido una relación muy filial y hemos involucrado a las sedes Atanasio Girardot en un encuentro lecto – escritor, Maria Concepción palacios y José Celestino Mutis en una prueba diagnostica para las pruebas saber.

La realización de estas jornadas aparte de encontrar estos espacios de recreación y buena utilización del tiempo libre, son espacios sociales donde se comparte, no solo a nivel de compañeros sino también, con los mismos padres de familia, logrando con ello una mayor unión a nivel familiar.

NS. PAOLA ANDREA GIRALDO O. - LIC. JUAN CARLOS ZAPATA S.