Effetti termici nella metrologia a coordinate

La norma UNI EN ISO 10360-2:2010 prescrive: “I limiti per le condizioni ambientali ammesse che possono avere influenza sulle misurazioni, quali condizioni di temperatura, umidità dell’aria e vibrazione nel luogo di installazione, devono essere specificati: - dal fabbricante, nel caso di prove di accettazione; - dall’utilizzatore, nel caso di prove di riverifica periodica. In entrambi i casi, l'utilizzatore è libero di scegliere le condizioni ambientali nelle quali saranno eseguite le prove secondo la ISO 10360-2, all'interno dei limiti specificati.” La presente Guida si prefigge l’obiettivo di rendere disponibile all’utilizzatore di Macchine di Misura a Coordinate (di seguito CMM) una serie di indicazioni e informazioni relative principalmente alla grandezza di influenza temperatura ed ai suoi effetti nelle misurazioni dimensionali. Affinché si possano ottenere le prestazioni dichiarate sui cataloghi, il costruttore di CMM dichiara, insieme alle specifiche tecniche della macchina, anche alcuni parametri ambientali che ritiene debbano essere mantenuti entro i limiti specificati.Ci si trova quindi subito di fronte al dilemma: • Si è in grado di rispettare le condizioni ambientali prescritte? • oppure si può soprassedere ed accontentarsi di prestazioni finali diverse? E quali saranno queste nuove prestazioni? Alle prime domande ne seguono altre: • serve ottenere dalla macchina il massimo delle prestazioni dichiarate dal Costruttore oppure ci si può accontentare di qualcosa in meno? • Tutte le volte che si effettuano misurazioni si è in grado di ricondurre i risultati delle misurazioni alla temperatura di riferimento? Nel prossimo paragrafo vengono proposte alcune problematiche che sono frequentemente oggetto di domande da parte degli utilizzatori di CMM e alle quali la presente guida propone delle risposte, frutto di analisi ed esperienze maturate da coloro che hanno redatto articoli nelle riviste di settore. Il capitolo 2 indica quali sono i riferimenti per terminologia e definizioni. I capitoli 3, 4, 5, 6, 7 e 8 sono il corpo centrale della guida e descrivono il fenomeno temperatura da un punto di vista fisico. Il capitolo 9 presenta invece un'ampia bibliografia comprendendo nel contempo termini di riferimenti normativi, nonché articoli scritti da esperti del settore in vari ambiti: tutto ciò allo scopo di fornire materiale utile sia per un approfondimento dei temi trattati nella stessa guida, sia per supportare (grazie soprattutto alle esperienze già maturate e descritte nei vari articoli) coloro i quali si trovassero ad affrontare per la prima volta simili tematiche

Metabolic reprogramming promotes myogenesis during aging

Sarcopenia is the age-related progressive loss of skeletal muscle mass and strength finally leading to poor physical performance. Impaired myogenesis contributes to the pathogenesis of sarcopenia, while mitochondrial dysfunctions are thought to play a primary role in skeletal muscle loss during aging. Here we studied the link between myogenesis and metabolism. In particular, we analyzed the effect of the metabolic modulator trimetazidine (TMZ) on myogenesis in aging. We show that reprogramming the metabolism by TMZ treatment for 12 consecutive days stimulates myogenic gene expression in skeletal muscle of 22-month-old mice. Our data also reveal that TMZ increases the levels of mitochondrial proteins and stimulates the oxidative metabolism in aged muscles, this finding being in line with our previous observations in cachectic mice. Moreover, we show that, besides TMZ also other types of metabolic modulators (i.e., 5-Aminoimidazole-4-Carboxamide Ribofuranoside-AICAR) can stimulate differentiation of skeletal muscle progenitors in vitro. Overall, our results reveal that reprogramming the metabolism stimulates myogenesis while triggering mitochondrial proteins synthesis in vivo during aging. Together with the previously reported ability of TMZ to increase muscle strength in aged mice, these new data suggest an interesting non-invasive therapeutic strategy which could contribute to improving muscle quality and neuromuscular communication in the elderly, and counteracting sarcopenia

Modulating the metabolism by trimetazidine enhances myoblast differentiation and promotes myogenesis in cachectic tumor-bearing c26 mice.

Trimetazidine (TMZ) is a metabolic reprogramming agent able to partially inhibit mitochondrial free fatty acid β-oxidation while enhancing glucose oxidation. Here we have found that the metabolic shift driven by TMZ enhances the myogenic potential of skeletal muscle progenitor cells leading to MyoD, Myogenin, Desmin and the slow isoforms of troponin C and I over-expression. Moreover, similarly to exercise, TMZ stimulates the phosphorylation of the AMP-activated protein kinase (AMPK) and up-regulates the peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α), both of which are known to enhance the mitochondrial biogenesis necessary for myoblast differentiation. TMZ also induces autophagy which is required during myoblast differentiation and promotes myoblast alignment which allows cell fusion and myofiber formation. Finally, we found that intraperitoneally administered TMZ (5mg/kg) is able to stimulate myogenesis in vivo both in a mice model of cancer cachexia (C26 mice) and upon cardiotoxin damage. Collectively, our work demonstrates that TMZ enhances myoblast differentiation and promotes myogenesis, which might contribute recovering stem cell blunted regenerative capacity and counteracting muscle wasting, thanks to the formation of new myofibers; TMZ is already in use in humans as an anti-anginal drug and its repositioning might impact significantly on aging and regeneration-impaired disorders, including cancer cachexia, as well as have implications in regenerative medicine

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia