De l'antropologia a l'educació. Una lectura des de Margaret Mead

En el presente artículo se ensaya una aproximación a la obra de la antropóloga Margaret Mead en clave pedagógica. Siendo así que se muestra una interpretación sobre sus pensamientos alrededor de la educación a partir de los estudios, comentarios y opiniones sobre los sistemas educativos, relaciones educativas y procesos de enseñanza aprendizaje que se explicitan, reiteradamente, a lo largo de su obra. A fin de cuentas, y como la propia autora indicaba, estudiar la educación era implícitamente necesario a todo estudio antropológico. Concepción que la llevó a incluir en la mayor parte de sus estudios, variables de análisis educativos, llegando incluso a centralizar la atención en este ámbito como idea central de algunos de sus escritos. Añadir además que, en esta síntesis se ha optado por presentar la evolución de su pensamiento pedagógico en base a momentos singulares y carismáticos, mostrando así las distintas continuidades y discontinuidades de su pensamiento. _____________________________________________________________________________________________________________________________________________________________________________ La présente étude tente une approche de l’oeuvre de l’anthropologue Margaret Mead dans une perspective pédagogique. C’est ainsi qu’est présentée une interprétation sur ses réflexions autour de l’éducation à partir des études, commentaires et opinions sur les systèmes éducatifs, des relations éducatives et des processus d’enseignementapprentissage qui sont explicités, de manière réitérée, tout au long de son oeuvre. En fin de compte, et comme l’auteur elle-même l’indiquait, étudier l’éducation était implicitement nécessaire à toute étude anthropologique. C’est une conception qui l’entraîna d’ailleurs à inclure dans la plupart de ses études des variables d’analyses éducatives, en parvenant même à centrer l’attention sur ce domaine comme idée centrale de certains de ses écrits. Il faut en outre ajouter que l’on a opté, dans cette synthèse, pour présenter l’évolution de sa pensée pédagogique sur la base de moments singuliers et exceptionnels, montrant ainsi les différentes continuités et discontinuités de sa pensée.The present article considers the work of the anthropologist Margaret Mead from an educational perspective. Thus, it offers an interpretation of her ideas on education through reference to the studies, comments and opinions regarding school systems, educational relationships and teaching/learning processes that appear repeatedly throughout her work. After all, and as the author herself pointed out, the study of education is implicitly required by every anthropological study, and this notion led her to include educational variables in most of her research; indeed, some of her writings take this aspect as their focus. The present review opts to present the development of her educational ideas according to key and charismatic features, thus revealing the various continuities and discontinuities in her thinking.En el presente artículo se ensaya una aproximación a la obra de la antropóloga Margaret Mead en clave pedagógica. Siendo así que se muestra una interpretación sobre sus pensamientos alrededor de la educación a partir de los estudios, comentarios y opiniones sobre los sistemas educativos, relaciones educativas y procesos de enseñanza aprendizaje que se explicitan, reiteradamente, a lo largo de su obra. A fin de cuentas, y como la propia autora indicaba, estudiar la educación era implícitamente necesario a todo estudio antropológico. Concepción que la llevó a incluir en la mayor parte de sus estudios, variables de análisis educativos, llegando incluso a centralizar la atención en este ámbito como idea central de algunos de sus escritos. Añadir además que, en esta síntesis se ha optado por presentar la evolución de su pensamiento pedagógico en base a momentos singulares y carismáticos, mostrando así las distintas continuidades y discontinuidades de su pensamiento

Comparative gene expression profiling between human cultured myotubes and skeletal muscle tissue

<p>Abstract</p> <p>Background</p> <p>A high-sensitivity DNA microarray platform requiring nanograms of RNA input facilitates the application of transcriptome analysis to individual skeletal muscle (SM) tissue samples. Culturing myotubes from SM-biopsies enables investigating transcriptional defects and assaying therapeutic strategies. This study compares the transcriptome of aneurally cultured human SM cells versus that of tissue biopsies.</p> <p>Results</p> <p>We used the Illumina expression BeadChips to determine the transcriptomic differences between tissue and cultured SM samples from five individuals. Changes in the expression of several genes were confirmed by QuantiGene Plex assay or reverse transcription real-time PCR. In cultured myotubes compared to the tissue, 1216 genes were regulated: 583 down and 633 up. Gene ontology analysis showed that downregulated genes were mainly associated with cytoplasm, particularly mitochondria, and involved in metabolism and the muscle-system/contraction process. Upregulated genes were predominantly related to cytoplasm, endoplasmic reticulum, and extracellular matrix. The most significantly regulated pathway was mitochondrial dysfunction. Apoptosis genes were also modulated. Among the most downregulated genes detected in this study were genes encoding metabolic proteins AMPD1, PYGM, CPT1B and UCP3, muscle-system proteins TMOD4, MYBPC1, MYOZ1 and XIRP2, the proteolytic CAPN3 and the myogenic regulator MYF6. Coordinated reduced expression of five members of the GIMAP gene family, which form a cluster on chromosome 7, was shown, and the GIMAP4-reduction was validated. Within the most upregulated group were genes encoding senescence/apoptosis-related proteins CDKN1A and KIAA1199 and potential regulatory factors HIF1A, TOP2A and CCDC80.</p> <p>Conclusions</p> <p>Cultured muscle cells display reductive metabolic and muscle-system transcriptome adaptations as observed in muscle atrophy and they activate tissue-remodeling and senescence/apoptosis processes.</p

Glucose and fructose have sugar-specific effects in both liver and skeletal muscle in vivo: a role for liver fructokinase.

We examined glucose and fructose effects on serine phosphorylation levels of a range of proteins in rat liver and muscle cells. For this, healthy adult rats were subjected to either oral glucose or fructose loads. A mini-array system was utilized to determine serine phosphorylation levels of liver and skeletal muscle proteins. A glucose oral load of 125 mg/100 g body weight (G 1/2) did not induce changes in phosphorylated serines of the proteins studied. Loading with 250 mg/100 g body weight of fructose (Fr), which induced similar glycemia levels as G 1/2, significantly increased serine phosphorylation of liver cyclin D3, PI3 kinase/p85, ERK-2, PTP2 and clusterin. The G 1/2 increased serine levels of the skeletal muscle proteins cyclin H, Cdk2, IRAK, total PKC, PTP1B, c-Raf 1, Ras and the β-subunit of the insulin receptor. The Fr induced a significant increase only in muscle serine phosphorylation of PI3 kinase/p85. The incubation of isolated rat hepatocytes with 10 mM glucose for 5 min significantly increased serine phosphorylation of 31 proteins. In contrast, incubation with 10 mM fructose produced less intense effects. Incubation with 10 mM glucose plus 75 µM fructose counteracted the effects of the incubation with glucose alone, except those on Raf-1 and Ras. Less marked effects were detected in cultured muscle cells incubated with 10 mM glucose or 10 mM glucose plus 75 µM fructose. Our results suggest that glucose and fructose act as specific functional modulators through a general mechanism that involves liver-generated signals, like micromolar fructosemia, which would inform peripheral tissues of the presence of either glucose- or fructose-derived metabolites

Expression of Glycogen Phosphorylase Isoforms in Cultured Muscle from Patients with McArdle's Disease Carrying the p.R771PfsX33 PYGM Mutation

Mutations in the PYGM gene encoding skeletal muscle glycogen phosphorylase (GP) cause a metabolic disorder known as McArdle's disease. Previous studies in muscle biopsies and cultured muscle cells from McArdle patients have shown that PYGM mutations abolish GP activity in skeletal muscle, but that the enzyme activity reappears when muscle cells are in culture. The identification of the GP isoenzyme that accounts for this activity remains controversial

Glucose and fructose have sugar-specific effects in both liver and skeletal muscle in vivo: a role for liver fructokinase.

We examined glucose and fructose effects on serine phosphorylation levels of a range of proteins in rat liver and muscle cells. For this, healthy adult rats were subjected to either oral glucose or fructose loads. A mini-array system was utilized to determine serine phosphorylation levels of liver and skeletal muscle proteins. A glucose oral load of 125 mg/100 g body weight (G 1/2) did not induce changes in phosphorylated serines of the proteins studied. Loading with 250 mg/100 g body weight of fructose (Fr), which induced similar glycemia levels as G 1/2, significantly increased serine phosphorylation of liver cyclin D3, PI3 kinase/p85, ERK-2, PTP2 and clusterin. The G 1/2 increased serine levels of the skeletal muscle proteins cyclin H, Cdk2, IRAK, total PKC, PTP1B, c-Raf 1, Ras and the β-subunit of the insulin receptor. The Fr induced a significant increase only in muscle serine phosphorylation of PI3 kinase/p85. The incubation of isolated rat hepatocytes with 10 mM glucose for 5 min significantly increased serine phosphorylation of 31 proteins. In contrast, incubation with 10 mM fructose produced less intense effects. Incubation with 10 mM glucose plus 75 µM fructose counteracted the effects of the incubation with glucose alone, except those on Raf-1 and Ras. Less marked effects were detected in cultured muscle cells incubated with 10 mM glucose or 10 mM glucose plus 75 µM fructose. Our results suggest that glucose and fructose act as specific functional modulators through a general mechanism that involves liver-generated signals, like micromolar fructosemia, which would inform peripheral tissues of the presence of either glucose- or fructose-derived metabolites

Regulation of glycogen metabolism in cultured human muscles by the glycogen phosphorylase inhibitor CP-91149.

Pharmacological inhibition of liver GP (glycogen phosphorylase), which is currently being studied as a treatment for Type II (non-insulin-dependent) diabetes, may affect muscle glycogen metabolism. In the present study, we analysed the effects of the GP inhibitor CP-91149 on non-engineered or GP-overexpressing cultured human muscle cells. We found that CP-91149 treatment decreased muscle GP activity by (1) converting the phosphorylated AMP-independent a form into the dephosphorylated AMP-dependent b form and (2) inhibiting GP a activity and AMP-mediated GP b activation. Dephosphorylation of GP was exerted, irrespective of incubation of the cells with glucose, whereas inhibition of its activity was synergic with glucose. As expected, CP-91149 impaired the glycogenolysis induced by glucose deprivation. CP-91149 also promoted the dephosphorylation and activation of GS (glycogen synthase) in non-engineered or GP-overexpressing cultured human muscle cells, but exclusively in glucose-deprived cells. However, this inhibitor did not activate GS in glucose-deprived but glycogen-replete cells overexpressing PTG (protein targeting to glycogen), thus suggesting that glycogen inhibits the CP-91149-mediated activation of GS. Consistently, CP-91149 promoted glycogen resynthesis, but not its overaccumulation. Hence, treatment with CP-91149 impairs muscle glycogen breakdown, but enhances its recovery, which may be useful for the treatment of Type II (insulin-dependent) diabetes