Colaboración entre dos facultades de veterinaria para la elaboración de material anatómico biblingüe en formato digital

[SPA]Se recopilan en este trabajo las actividades de colaboración entre la Facultad de Veterinaria de Murcia (área de Anatomía Veterinaria) y el Royal Veterinary College de Londres (E-media y Anatomy units) para la elaboración de diferentes recursos docentes on-line en formato bilingüe. Se trata de una experiencia de 4 años, en la que se han implicado tanto el profesorado como algunos alumnos. Durante este tiempo se han elaborado diversos programas interactivos basados en la identificación de estructuras sobre imágenes, así como contenidos en formato vídeo (podcasts). Otra vertiente del trabajo ha consistido en colaborar en el desarrollo de una Wiki específica de Veterinaria (WikiVet, http://en.wikivet.net/Veterinary_Education_Online). En este sentido, destaca la reciente creación de la versión de dicha Wiki en lengua española (http://es.wikivet.net/P%C3%A1gina_Principal). Todo el material se ha venido incluyendo en los entornos educativos virtuales de cada institución (SUMA y Blackboard), así como en la web del área de Anatomía Veterinaria http://www.um.es/anatvet/interactivo.php. La experiencia llevada a cabo se ha mostrado como un medio efectivo para la innovación docente en disciplinas de carácter morfológico como la Anatomía. Además, la producción de material en versión bilingüe ha supuesto una enriquecedora experiencia profesional, a la vez que un mayor número de potenciales usuarios. [ENG]This study summarizes the collaborative activities between the Faculty of Veterinary of Murcia (area of Veterinary Anatomy) and the Royal Veterinary College London (E-media and Anatomy units) for the development of different online teaching resources in a bilingual format. This 4 year experience involved faculty lecturers, students and technical staff. Interactive programs based on the identification of landmarks over images as well as podcast with practical demonstrations have been developed. The collaboration was also aimend at developing the Spanish version of the WikiVet (http://es.wikivet.net/P%C3%A1gina_Principal). All the materials were uploaded in virtual learning environments of each institution (SUMA and Blackboard), as well as on the web site of the Veterinary Anatomy (open http://www.um.es/anatvet/ingles/interactive.php. The experience has been proved to be an effective means for innovative teaching in morphology areas as Anatomy. Also, the production of bilingual versions of each resource has provided an enriching experience for teachers and given a greater number of potential users.Campus Mare Nostrum, Universidad Politécnica de Cartagena, Universidad de Murcia, Región de Murci

Symmorphosis through dietary regulation: a combinatorial role for proteolysis, autophagy and protein synthesis in normalising muscle metabolism and function of hypertrophic mice after acute starvation

Animals are imbued with adaptive mechanisms spanning from the tissue/organ to the cellular scale which insure that processes of homeostasis are preserved in the landscape of size change. However we and others have postulated that the degree of adaptation is limited and that once outside the normal levels of size fluctuations, cells and tissues function in an aberant manner. In this study we examine the function of muscle in the myostatin null mouse which is an excellent model for hypertrophy beyond levels of normal growth and consequeces of acute starvation to restore mass. We show that muscle growth is sustained through protein synthesis driven by Serum/Glucocorticoid Kinase 1 (SGK1) rather than Akt1. Furthermore our metabonomic profiling of hypertrophic muscle shows that carbon from nutrient sources is being channelled for the production of biomass rather than ATP production. However the muscle displays elevated levels of autophagy and decreased levels of muscle tension. We demonstrate the myostatin null muscle is acutely sensitive to changes in diet and activates both the proteolytic and autophagy programmes and shutting down protein synthesis more extensively than is the case for wild-types. Poignantly we show that acute starvation which is detrimental to wild-type animals is beneficial in terms of metabolism and muscle function in the myostatin null mice by normalising tension production

Testing the functional integrity of ocular reflexes

This Flash simulation from the Royal Veterinary College is designed to help pre-clinical students to understand the function of ocular nerves and muscles. The student is presented with a virtual patient to test pupillary (consensual) light reflex, palpebral and corneal reflexes as well as testing the nervous control of extra-ocular muscles of the eye. This provides a safe way to observe and practice on a wide range of nerve or ocular deficits and also receive informative feedback.

Exercise training attenuates the hypermuscular phenotype and restores skeletal muscle function in the myostatin null mouse

Myostatin regulates both muscle mass and muscle metabolism. The myostatin null (MSTN -/- ) mouse has a hypermuscular phenotype owing to both hypertrophy and hyperplasia of the myofibres. The enlarged muscles display a reliance on glycolysis for energy production; however, enlarged muscles that develop in the absence of myostatin have compromised force-generating capacity. Recent evidence has suggested that endurance exercise training increases the oxidative properties of muscle. Here, we aimed to identify key changes in the muscle phenotype of MSTN -/- mice that can be induced by training. To this end, we subjected MSTN -/- mice to two different forms of training, namely voluntary wheel running and swimming, and compared the response at the morphological, myocellular and molecular levels. We found that both regimes normalized changes of myostatin deficiency and restored muscle function. We showed that both exercise training regimes increased muscle capillary density and the expression of Ucp3, Cpt1α, Pdk4 and Errγ, key markers for oxidative metabolism. Cross-sectional area of hypertrophic myofibres from MSTN -/- mice decreased towards wild-type values in response to exercise and, in this context, Bnip3, a key autophagy-related gene, was upregulated. This reduction in myofibre size caused an increase of the nuclear-to-cytoplasmic ratio towards wild-type values. Importantly, both training regimes increased muscle force in MSTN -/- mice. We conclude that impaired skeletal muscle function in myostatin-deficient mice can be improved through endurance exercise-mediated remodelling of muscle fibre size and metabolic profile. © 2011 The Authors. Experimental Physiology © 2012 The Physiological Society

Propeptide-mediated inhibition of myostatin increases muscle mass through inhibiting proteolytic pathways in aged mice

Mammalian aging is accompanied by a progressive loss of skeletal muscle, a process called sarcopenia. Myostatin, a secreted member of the transforming growth factor-β family of signaling molecules, has been shown to be a potent inhibitor of muscle growth. Here, we examined whether muscle growth could be promoted in aged animals by antagonizing the activity of myostatin through the neutralizing activity of the myostatin propeptide. We show that a single injection of an AAV8 virus expressing the myostatin propeptide induced an increase in whole body weights and all muscles examined within 7 weeks of treatment. Our cellular studies demonstrate that muscle enlargement was due to selective fiber type hypertrophy, which was accompanied by a shift toward a glycolytic phenotype. Our molecular investigations elucidate the mechanism underpinning muscle hypertrophy by showing a decrease in the expression of key genes that control ubiquitin-mediated protein breakdown. Most importantly, we show that the hypertrophic muscle that develops as a consequence of myostatin propeptide in aged mice has normal contractile properties. We suggest that attenuating myostatin signaling could be a very attractive strategy to halt and possibly reverse age-related muscle loss

Changes in body mass in wild-type (WT) and <i>Mstn</i>^{<i>−/−</i>} (Mstn) at 12 and 24 hours after complete food withdrawal (acute starvation).

<p>(A) Wild-type mice showed a significant decrease after 24h starvation. In contrast <i>Mstn</i>^{<i>−/−</i>} lost mass in the first and second 12h of starvation. (B) Changes in body weight expressed as a % of normal body weight. Weight changes of (C) EDL, (D) soleus, (E) TA and (F) Gastrocnemius at 12 and 24h after acute starvation. Wild-type animals showed no significant muscle mass reduction in contrast to all muscles examined from <i>Mstn</i>^{<i>−/−</i>}. (Two-way ANOVA; *p<0.05)</p

Expression of SGK1 in wild-type and <i>Mstn</i>^{<i>−/−</i>} Tibialis Anterior (TA) before and after acute 24 starvation.

<p>(A) Western blot and scanning densitometry analysis of 54kD band. (B) (D) Altered profile of SGK1 expression in IIB fibres of <i>Mstn</i>^{<i>−/−</i>} TA muscle. (C) Immunochemistry for the expression of MCH IIB and SGK1 (Scale bar = 100μm). (E) Western blot analysis of phosphorylated FoxO3a at residues T32 and S253 from the TA muscles and the influence of starvation. Phosphorylation at T32 indicated by arrow marking the upper band. (F) Quantification of pFoxO3a-T32/ FoxO3a (Two-way ANOVA; *p<0.05).</p

Evidence that a maternal "junk food" diet during pregnancy and lactation can reduce muscle force in offspring

Obesity is a multi-factorial condition generally attributed to an unbalanced diet and lack of exercise. Recent evidence suggests that maternal malnutrition during pregnancy and lactation can also contribute to the development of obesity in offspring. We have developed an animal model in rats to examine the effects of maternal overeating on a westernised "junk food" diet using palatable processed foods rich in fat, sugar and salt designed for human consumption. Using this model, we have shown that such a maternal diet can promote overeating and a greater preference for junk food in offspring at the end of adolescence. The maternal junk food diet also promoted adiposity and muscle atrophy at weaning. Impaired muscle development may permanently affect the function of this tissue including its ability to generate force. The aim of this study is to determine whether a maternal junk food diet can impair muscle force generation in offspring. Twitch and tetanic tensions were measured in offspring fed either chow alone (C) or with a junk food diet (J) during gestation, lactation and/or post-weaning up to the end of adolescence such that three groups of offspring were used, namely the CCC, JJC and JJJ groups. We show that adult offspring from mothers fed the junk food diet in pregnancy and lactation display reduced muscle force (both specific twitch and tetanic tensions) regardless of the post-weaning diet compared with offspring from mothers fed a balanced diet. Maternal malnutrition can influence muscle force production in offspring which may affect an individual's ability to exercise and thereby combat obesity