La gestión de la innovación como la gestión de un ecosistema heterogéneo y estructurado

[ES] Este artículo aborda la innovación como un proceso evolutivo que toma lugar en un ecosistema heterogéneo estructurado. Esto permite entender la gestión de la innovación como la gestión de las interacciones en un ecosistema que se quiere modificar.

Del miedo a la obesidad a la obsesión por la delgadez; actitudes y dieta

Este trabajo se encuentra bajo la licencia Creative Commons Attribution 3.0.

Efecto de la calidad de la dieta sobre las eficiencias de selección y absorción del alimento en semillas de mejillón de crecimiento rápido y lento

INGLÉS:Juvenile mussels (Mytilus galloprovincialis) were collected and maintained under restrictive and optimal feeding conditions. After 7 months maintenance fast and slow growth individuals were selected for study of the effect of diet quality on selection efficiencies and absorption of food in fast and slow growth mussels. The objective of this experiment was to confirm that the physiological components responsible for the differentiation were able to vary according to the environmental conditions. The analysis of physiological traits indicates that under conditions of abundant food efficiency and absorption efficiences are the main factors that explain the differences in growth. Under conditions of restricted food are physiological differences that give rise to differences in growth.

Muscle wasting in myotonic dystrophies: a model of premature aging

Myotonic dystrophy type 1 (DM1 or Steinert's disease) and type 2 (DM2) are multisystem disorders of genetic origin. Progressive muscular weakness, atrophy and myotonia are the most prominent neuromuscular features of these diseases, while other clinical manifestations such as cardiomyopathy, insulin resistance and cataracts are also common. From a clinical perspective, most DM symptoms are interpreted as a result of an accelerated aging (cataracts, muscular weakness and atrophy, cognitive decline, metabolic dysfunction, etc.), including an increased risk of developing tumors. From this point of view, DM1 could be described as a progeroid syndrome since a notable age dependent dysfunction of all systems occurs. The underlying molecular disorder in DM1 consists of the existence of a pathological (CTG) triplet expansion in the 3' untranslated region (UTR) of the Dystrophia ll/Iyotonica Protein Kinase (DMPK) gene, whereas (CCTG)n repeats in the first intron of the Cellular Nucleic acid Binding Protein/Zinc Finger Protein 9 (CNBP/ZNF9) gene cause DM2. The expansions are transcribed into (CUG)n and (CCUG)n-containing RNA, respectively, which form secondary structures and sequester RNA binding proteins, such as the splicing factor muscleblind-like protein (MBNL), forming nuclear aggregates known as foci. Other splicing factors, such as CUGBP, are also disrupted, leading to a spliceopathy of a large number of downstream genes linked to the clinical features of these diseases. Skeletal muscle regeneration relies on muscle progenitor cells, known as satellite cells, which are activated after muscle damage, and which proliferate and differentiate to muscle cells, thus regenerating the damaged tissue. Satellite cell dysfunction seems to be a common feature of both age-dependent muscle degeneration (sarcopenia) and muscle wasting in DM and other muscle degenerative diseases. This review aims to describe the cellular, molecular and macrostructural processes involved in the muscular degeneration seen in DM patients, highlighting the similarities found with muscle aging.