1,572 research outputs found

    Nutrition and microRNAs: Novel Insights to Fight Sarcopenia

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    Sarcopenia is a progressive age-related loss of skeletal muscle mass and strength, which may result in increased physical frailty and a higher risk of adverse events. Low-grade systemic inflammation, loss of muscle protein homeostasis, mitochondrial dysfunction, and reduced number and function of satellite cells seem to be the key points for the induction of muscle wasting, contributing to the pathophysiological mechanisms of sarcopenia. While a range of genetic, hormonal, and environmental factors has been reported to contribute to the onset of sarcopenia, dietary interventions targeting protein or antioxidant intake may have a positive effect in increasing muscle mass and strength, regulating protein homeostasis, oxidative reaction, and cell autophagy, thus providing a cellular lifespan extension. MicroRNAs (miRNAs) are endogenous small non-coding RNAs, which control gene expression in different tissues. In skeletal muscle, a range of miRNAs, named myomiRNAs, are involved in many physiological processes, such as growth, development, and maintenance of muscle mass and function. This review aims to present and to discuss some of the most relevant molecular mechanisms related to the pathophysiological effect of sarcopenia. Besides, we explored the role of nutrition as a possible way to counteract the loss of muscle mass and function associated with ageing, with special attention paid to nutrient-dependent miRNAs regulation. This review will provide important information to better understand sarcopenia and, thus, to facilitate research and therapeutic strategies to counteract the pathophysiological effect of ageing

    Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications

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    With advancing aging, a decline in physical abilities occurs, leading to reduced mobility and loss of independence. Although many factors contribute to the physio-pathological effects of aging, an important event seems to be related to the compromised integrity of the neuromuscular system, which connects the brain and skeletal muscles via motoneurons and the neuromuscular junctions (NMJs). NMJs undergo severe functional, morphological, and molecular alterations during aging and ultimately degenerate. The effect of this decline is an inexorable decrease in skeletal muscle mass and strength, a condition generally known as sarcopenia. Moreover, several studies have highlighted how the age-related alteration of reactive oxygen species (ROS) homeostasis can contribute to changes in the neuromuscular junction morphology and stability, leading to the reduction in fiber number and innervation. Increasing evidence supports the involvement of epigenetic modifications in age-dependent alterations of the NMJ. In particular, DNA methylation, histone modifications, and miRNA-dependent gene expression represent the major epigenetic mechanisms that play a crucial role in NMJ remodeling. It is established that environmental and lifestyle factors, such as physical exercise and nutrition that are susceptible to change during aging, can modulate epigenetic phenomena and attenuate the age-related NMJs changes. This review aims to highlight the recent epigenetic findings related to the NMJ dysregulation during aging and the role of physical activity and nutrition as possible interventions to attenuate or delay the age-related decline in the neuromuscular system

    Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration

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    Skeletal muscle is characterized by a remarkable capacity to rearrange after physiological changes and efficiently regenerate. However, during aging, extensive injury, or pathological conditions, the complete regenerative program is severely affected, with a progressive loss of muscle mass and function, a condition known as sarcopenia. The compromised tissue repair program is attributable to the gradual depletion of stem cells and to altered regulatory signals. Defective muscle regeneration can severely affect re-innervation by motor axons, and neuromuscular junctions (NMJs) development, ultimately leading to skeletal muscle atrophy. Defects in NMJ formation and maintenance occur physiologically during aging and are responsible for the pathogenesis of several neuromuscular disorders. However, it is still largely unknown how neuromuscular connections are restored on regenerating fibers. It has been suggested that attractive and repelling signals used for axon guidance could be implicated in this process; in particular, guidance molecules called semaphorins play a key role. Semaphorins are a wide family of extracellular regulatory signals with a multifaceted role in cell-cell communication. Originally discovered as axon guidance factors, they have been implicated in cancer progression, embryonal organogenesis, skeletal muscle innervation, and other physiological and developmental functions in different tissues. In particular, in skeletal muscle, specific semaphorin molecules are involved in the restoration and remodeling of the nerve-muscle connections, thus emphasizing their plausible role to ensure the success of muscle regeneration. This review article aims to discuss the impact of aging on skeletal muscle regeneration and NMJs remodeling and will highlight the most recent insights about the role of semaphorins in this context

    Lettera di Alessandra

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    Un ritratto critico dell'opera di Alessandra Carnaroli, autrice fra le più apprezzate delle ultime generazioni della poesia di ricerca. La sezione a lei dedicata, nel numero della rivista, contiene inoltre saggi di Cecilia Bello Minciacchi, Andrea Cortellessa, e Ivan Schiavone; e vari inediti dell'autrice. Il saggio è pubblicato con lo pseudonimo di Tommaso Ottonieri.A critical portrait of the work of Alessandra Carnaroli, author of the most appreciated in the latest generations of italian research poetry. Published under the pseudonym Tommaso Ottonieri

    Selected letters of Alessandra Strozzi

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    The letters of Alessandra Strozzi provide a vivid and spirited portrayal of life in fifteenth-century Florence. Among the richest autobiographical materials to survive from the Italian Renaissance, the letters reveal a woman who fought stubbornly to preserve her family's property and position in adverse circumstances, and who was an acute observer of Medicean society. Her letters speak of political and social status, of the concept of honor, and of the harshness of life, including the plague and the loss of children. They are also a guide to Alessandra's inner life over a period of twenty-three years, revealing the pain and sorrow, and, more rarely, the joy and triumph, with which she responded to the events unfolding around her.This edition includes translations, in full or in part, of 35 of the 73 extant letters. The selections carry forward the story of Alessandra's life and illustrate the range of attitudes, concerns, and activities which were characteristic of their author

    Challenging the author: Gavin Douglas's Eneados

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    Gavin Douglas’s Eneados, a translation into the “Scottis” tongue of Virgil’s Aeneid, completed in 1513 and first published in London in 1553, presents, as well as the translation of the additional thirteenth book by Maphaeus Vegius, original prologues and marginal notes to the text, rubrics and articulate conclusive material. The present paper analyses this complex paratext as evidence of Douglas’s almost philological attention to the original and his preoccupation with a faithful reproduction; it is also suggested that the models for his organization of the commentary might be both medieval (i.e., manuscripts such as Petrarch’s Virgilius Ambrosianus) and early modern, as in the case of editions of classical works: the most apt example being Jodocus Badius Ascensius’ edition of the Aeneid, printed in 1501. The Eneados thus stands on the threshold between manuscript and print, and might have indicated new possibilities of use of the printing medium in Scotland, and of the value of the translation of a classical text, had history not intervened with the Scottish defeat at Flodden Fields in 1513, which put a temporary stop both to the circulation of the Eneados and to the development of Scottish printing

    Inhibition of phosphoinositide 3-kinase/protein kinase B signaling hampers the vasopressin-dependent stimulation of myogenic differentiation

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    Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways. The AVP system is impaired in several neuromuscular diseases, suggesting that AVP may act as a physiological factor in skeletal muscle. Since the Phosphoinositide 3-kinases/Protein Kinase B/mammalian Target Of Rapamycin (PI3K/Akt/mTOR) signaling plays a significant role in regulating muscle mass, we evaluated its role in the AVP myogenic effect. In L6 cells AKT1 expression was knocked down, and the AVP-dependent expression of mTOR and Forkhead box O3 (FoxO) was analyzed by Western blotting. The effect of the PI3K inhibitor LY294002 was evaluated by cellular and molecular techniques. Akt knockdown hampered the AVP-dependent mTOR expression while increased the levels of FoxO transcription factor. LY294002 treatment inhibited the AVP-dependent expression of Myocyte Enhancer Factor-2 (MEF2) and myogenin and prevented the nuclear translocation of MEF2. LY294002 also repressed the AVP-dependent nuclear export of histone deacetylase 4 (HDAC4) interfering with the formation of multifactorial complexes on the myogenin promoter. We demonstrate that the PI3K/Akt pathway is essential for the full myogenic effect of AVP and that, by targeting this pathway, one may highlight novel strategies to counteract muscle wasting in aging or neuromuscular disorders

    Semaphorins: missing signals in age-dependent alteration of neuromuscular junctions and skeletal muscle regeneration

    No full text
    : Skeletal muscle is characterized by a remarkable capacity to rearrange after physiological changes and efficiently regenerate. However, during aging, extensive injury, or pathological conditions, the complete regenerative program is severely affected, with a progressive loss of muscle mass and function, a condition known as sarcopenia. The compromised tissue repair program is attributable to the gradual depletion of stem cells and to altered regulatory signals. Defective muscle regeneration can severely affect re-innervation by motor axons, and neuromuscular junctions (NMJs) development, ultimately leading to skeletal muscle atrophy. Defects in NMJ formation and maintenance occur physiologically during aging and are responsible for the pathogenesis of several neuromuscular disorders. However, it is still largely unknown how neuromuscular connections are restored on regenerating fibers. It has been suggested that attractive and repelling signals used for axon guidance could be implicated in this process; in particular, guidance molecules called semaphorins play a key role. Semaphorins are a wide family of extracellular regulatory signals with a multifaceted role in cell-cell communication. Originally discovered as axon guidance factors, they have been implicated in cancer progression, embryonal organogenesis, skeletal muscle innervation, and other physiological and developmental functions in different tissues. In particular, in skeletal muscle, specific semaphorin molecules are involved in the restoration and remodeling of the nerve-muscle connections, thus emphasizing their plausible role to ensure the success of muscle regeneration. This review article aims to discuss the impact of aging on skeletal muscle regeneration and NMJs remodeling and will highlight the most recent insights about the role of semaphorins in this context

    Nicetas Nicaenus, De azymis

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    The RAP online repertorium offers the first comprehensive catalogue of polemical literature related to the schism between the Roman Catholic and Orthodox Churches from the 9th to the 16th century and can be described as an ideal continuation of the *Clavis Patrum*. Each entry identifies the work (often unpublished or newly discovered in manuscript catalogs), lists its various titles (since medieval texts often lack stable titles), provides incipit and explicit (with possible variations), and examines the manuscript tradition and foliation (by reviewing catalogs or manuscripts, verifying dates, folios, etc.). It also includes relevant bibliography (critical editions and studies), identifies the author (using prosopographical studies, dictionaries, repertories, sigillography, etc.), and provides essential biographical details. Each work is classified by literary genre (e.g., treatise, dialogue), the corresponding Byzantine term, and the main polemical themes (e.g., Filioque, Azymes, Purgatory), and is assigned a unique RAP identification number. The Repertorium Auctorum Polemicorum is identified by the International Standard Serial Number (ISSN) 3035-2096 [continuously updated publication

    Polemica scripta anonyma, Dialogus inter Graecum et Cardinales quosdam de processione Spiritus Sancti

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    The RAP online repertorium offers the first comprehensive catalogue of polemical literature related to the schism between the Roman Catholic and Orthodox Churches from the 9th to the 16th century and can be described as an ideal continuation of the *Clavis Patrum*. Each entry identifies the work (often unpublished or newly discovered in manuscript catalogs), lists its various titles (since medieval texts often lack stable titles), provides incipit and explicit (with possible variations), and examines the manuscript tradition and foliation (by reviewing catalogs or manuscripts, verifying dates, folios, etc.). It also includes relevant bibliography (critical editions and studies), identifies the author (using prosopographical studies, dictionaries, repertories, sigillography, etc.), and provides essential biographical details. Each work is classified by literary genre (e.g., treatise, dialogue), the corresponding Byzantine term, and the main polemical themes (e.g., Filioque, Azymes, Purgatory), and is assigned a unique RAP identification number. The Repertorium Auctorum Polemicorum is identified by the International Standard Serial Number (ISSN) 3035-2096 [continuously updated publication
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