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1Department of Surgery, Oncology and Gastroenterology, Padua University Hospital, Padua,Italy
2 Department of Biomedical Sciences, University of Padua, Italy
3 CIR MYO -Interdepartmental Research Centre of Myology, University of Pdua, Italy
4
Armando &Carmela Mioni-Carraro Foundation for Translational Myology, Padua, Italy
✉
Department of Surgery, Oncology and Gastroenterology, Padova University Hospital, Padua, Italy. ORCID iD: 0000-0001-6070-0011 sanzamp@unipd.it
Conflict of Interest
The authors disclose no conflicts of research and publication interest or any specific endorsements of the products referenced in this manuscript.
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
Roles
Ugo Carraro: ORCID: 0000-0002-0924-4998
Received 2023 Mar 3; Accepted 2023 Mar 3; Collection date 2023 Mar 29.
This article is distributed under the terms of the Creative Commons Attribution Noncommercial License (by-nc 4.0) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
The 2023 Padua Days of Muscle and Mobility Medicine (Pdm3) are scheduled from March 29th to April 1st, 2023. The abstracts collected during autumn and early winter of 2022 were e-published in the issue 33(1) 2023 of the European Journal of Translational Myology (EJTM). Now the last-minute abstracts are reported here (100 Oral presentations are listed in the final Program). All together they confirm the interest of very different international specialists, filling the four days of 2023Pdm3. Indeed, scientists and clinicians from Austria, Bulgaria, Canada, Denmark, France, Georgia, Germany, Iceland, Ireland, Italy, Mongolia, Norway, Russia, Slovakia, Slovenia, Spain, Switzerland, The Netherlands and USA will gather to the Hotel Petrarca of Thermae of Euganean Hills, Padua, Italy. The apparent heterogeneity of the specialists, collectively raccolti under the umbrella of the Mobility Medicine neologism is stressed by the need to extend the Sections of the 2023 Editorial Borad of EJTM also here reported. We hope that Speakers of the 2023 Pdm3 and readers of EJTM will submit “Communications” to the European Journal of Translational Myology by May 20, 2023 and/or to the 2023 Special Issue: “Pdm3” of the Journal Diagnostics, MDPI, Basel, Switzerland with deadline September 30, 2023. See you soon at the Hotel Petrarca of Montegrotto Terme, Padua, Italy. For a promo of the 2023 Pdm3 link to: https://www.youtube.com/watch?v=zC02D4uPWRg
Key Words: Padua Days of Muscle and Mobility Medicine (Pdm3), last minute abstract, European Journal of Translational Myology and Mobility Medicine, PAGEpress, Pavia, Italy, Diagnostics, MDPI, Basel
Ethical Publication Statement
We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.
The Padua Muscle Days (PMDs), i.e., meetings ofbiology, physiology, medicine and rehabilitation of skeletal muscle started more than 30 years ago, precisely to provide advice on Translational Myology. Recently the interests broadened to complementary disciplines and neologisms were found necessary, specifically Mobility Medicine and the Padua Days of Muscle and Mobility Medicine (Pdm3). Despite the worsening evolution of the East-Europe crisis, the program of the 2023 Pdm3 was confirmed in autumn 2022 with Scientific Sessions to occur over four full days at either the Guariento Hall of the Galilean Academy of Arts, Letters and Sciences of Padua (March 29, 2023) and then in the Conference Hall of the Hotel Petrarca, Thermae of Euganean Hills (Padua), Italy. Collected during fall 2022, the titles and abstracts of approximately 90 oral presentations were listed in evolving preliminary schedules.1 Here we add 10 last-minute Abstracts, bringing the final Program to 100 Oral Presentations. The four days of 2023 Pdm3 will include senior and junior scientists and clinicians from Austria, Bulgaria, Canada, Denmark, France, Georgia, Germany, Iceland, Ireland, Italy, Mongolia, Norway, Russia, Slovakia, Slovenia, Spain, Switzerland, The Netherlands and USA. Together with the Final Programme, the two Collections of Abstracts are published in electronic format in issue 33(1) 2023 of the European Journal of Translational Myology (EJTM). The apparent heterogeneity of the specialists, gathered under the umbrella of the neologism Mobility Medicine, is underlined by the need to expand the Sections of the EJTM 2023 Editorial Board also reported here. In the two Complementary Collections some empty Abstracts appear with only names and affiliations of authors, due to the decision of the speakers not to disclose their unpublished results. It is a pity that this happens, but in the meantime, we stress that those decisions are strong evidence of the relevance of the 2023 Pdm3. Readers are invited to personally join the Meeting in Padua Galilean Academy of Arts, Letters and Sciences and in the Conference Hall of the Hotel Petrarca to get a preview of the original results of the best laboratories performing translational research on muscle and mobility medicine. See you in the late afternoon of March 28, 2023 for an aperitive at the Hotel Petrarca of Montegrotto Terme, Euganean Hills (Padua), Italy. We are confident that the 2023 Pdm3 will be as interesting as the successful events of the last years.2-14
For a promo of the 2023 Pdm3 link to: https://www.youtube.com/watch?v=zC02D4uPWRg
Finally, we would like to thank those organizers/chairs that were more able to attract speakers to the 2023 Pdma3, specifically: Elisabeth R. Barton, Ines Bersch-Porada, Paolo Gargiulo, Elena P. Ivanova, Christiaan Leeuwenburgh, Marco V. Narici, Riccardo Rosati, Piera Smeriglio, Carla Stecco, Daniela Tavian and H. Lee Sweeney.
Acknowledgments
The authors thank Organizers, Chairs, Speakers, and Attendees for their scientific and personal financial contributions to the success of the Pdm3.
List of acronyms
EJTM
European Journal of Translational Myology
MDPI
Molecular Diversity Preservation International
Pdm3
Padua Days on Muscle and Mobility Medicine
PMD
Padua Muscle Days
Funding Statement
Funding: The 2023 Pdm3 are supported by the University of Florida Myology Institute and Wellstone Center, Gainesville, FL, USA (H. Lee Sweeney, Gainesville, FL, USA) and by Physiko- & Rheuma-therapie, Institute for Physical Medicine and Rehabilitation, St. Pölten, Austria, Centre of Active Ageing - Competence Centre for Health, Prevention and Active Ageing, St. Pölten, Austria and Ludwig Boltzmann Institute for Rehabilitation Research, St. Pölten, Austria (Helmut Kern, Wien, Austria). E-publishing is supported by the Armando & Carmela Mioni-Carraro Foundation for Translational Myology, Padua, Italy.
References
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4, Laboratory Affiliated to Institute Pasteur Italia-Fondazione Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Rome, Italy
6 Scuola Superiore di Studi Avanzati Sapienza (SSAS), Sapienza University of Rome, Italy
1 Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy
2 Veneto Institute of Molecular Medicine, Padua, Italy
3 Department of Biomedical Sciences, University of Padua, Padua, Italy
4, Laboratory Affiliated to Institute Pasteur Italia-Fondazione Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Rome, Italy
5 Department of Neuroscience, Azienda Ospedaliera di Padova, Padua, Italy
6 Scuola Superiore di Studi Avanzati Sapienza (SSAS), Sapienza University of Rome, Italy
The global pandemic of coronavirus disease 2019 (COVID-19) has revealed a surprising number of extra-pulmonary manifestations of the SARS-CoV-2 infection. There have been emerging reports related to COVID-19 infection and disease course including myositis, neuropathy, arthropathy, and soft tissue abnormalities in lower and upper limb too. NMES can be used to induce a muscle contraction when it is difficult or impossible for the person to achieve this voluntarily thereby allowing effective exercise and the strengthening of muscles observed that usual programs for amyotrophy couldn’t provide any muscular contraction. So we propose specific neuro muscular electrostimulation (NMES) parameters at low frequency to increase upper limb muscles strength. We studied 10 patients who developed diffuse and symmetrical muscle weakness after a long stay in the intensive care unit (ICU). We applied 30 minutes a day for two months three different frequency electrostimulation to:
Arm extensor muscles because they provide help to the control of the trunk in sitting and standing position
Intrinsic muscles because of their severe ipotrophy.
We applied the following parameters of frequency:
Amyotrophy frequency 30-40 hz, 250 μs
Study frequency 1-2 hz, 250 μs
Triangular stimulation 0,2 hz, 250 μs
Muscle contractions have been detected by visualization and a biofeedback EMG device. In the arm extensor at the beginning only low Frequency and high intensive stimulation could provide muscle contraction. After two months of high intensive stimulation, and physiotherapy, muscle normal excitability seemed to be restored. About hand intrinsic muscle, triangle impulse resulted the best parameters. We treated very severe weak muscle in patient after long covid. In conclusion, to reanimate muscular function of arm extensor muscles, hypotrophy muscle stimulation tetanic parameters have not provide any muscular activity. Only low frequency (1-2 hz) high intensity stimulation (80-120 mAmp) could achieve muscular contraction.
LMNA-related disorders, or laminopathies, are rare diseases caused by mutations in the LMNA gene, which encodes for the nuclear envelope proteins, lamin A and C, via alternative splicing. The main functions of lamins are to provide structural support to the nucleus, maintenance of nuclear shape and spacing of nuclear pore complexes. Over the years, numerous reports have suggested that lamins also take part in other process: chromatin organization, DNA replication, epigenetics, transcription, cell cycle regulation, cell development and differentiation, nuclear migration, and apoptosis. Lamins together with integral membrane proteins of nuclear envelope and associated proteins participate in the regulation of chromatin organization and formation of chromatin microdomains associated with nuclear envelope. Laminopathies are associated with a wide range of disease phenotypes, including neuromuscular, cardiac, metabolic disorders and premature aging syndromes. Different phenotypes with skeletal muscle involvement have been linked to LMNA mutations: limb-girdle muscular dystrophy type 1B (LGMD1B, old nomenclature); autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD2) and the rarer recessive form (EDMD3), a form of congenital muscular dystrophy, the LMNA-related congenital muscular dystrophy (L-CMD). Although lamins A/C are expressed in almost all cells and tissues, the high degree of tissue-specificity (i.e., skeletal muscle, cardiac muscle, adipose tissue, peripheral nerve) and the resulting different phenotypes observed in laminopathies are not completely elucidated. Moreover, therapeutic approaches to laminopathies are as yet symptomatic and no cure is currently available for any of these diseases. These considerations provide evidence of the extent to which an Italian Network for Laminopathies (NIL), involving centers spread throughout Italy and involved in clinics, research, industry and patients and their associations can help in addressing the study of those diseases and finding a therapeutic strategy. The use of corticosteroids to improve muscle power in of patients withL-CMD has been proposed, despite to date there is no clear indications to support the use of corticosteroids in these patients and reliable biomarkers to demonstrate (or monitor) the effectiveness of the treatment is not available. Corticosteroids have anti-inflammatory activity and are able to modify the secretion of some cytokines. A study in a cohort of patients affected by muscular laminopathies found that TGF beta 2 secretion is consistently elevated in subjects with EDMD2 or other muscular laminopathies, except in L-CMD. Interestingly, our studies indicate that patients affected by L-CMD have a strongly altered profile of inflammatory cytokine secretion. This profile is also very different from that observed in patients affected by EDMD2, a form with later onset and slow progression of muscle disease. In fact, in L-CMD patients we observed an increase of interleukin 17, interleukin 9 and interleukin 1 receptor, whereas in patients with EDMD2 we reported a constant increase in TGFbeta 2 which was normal in L-CMD children. It is therefore reasonable to suppose that a different profile of the secretome may be related to the greater severity of the clinical picture of L-CMD. Starting from the collaborative approach and the multidisciplinary effort of the Italian Network for Laminopathies, we are performing an open-label prospective cohort pilot study to evaluate the effect of the treatment with Deflazacort in a cohort of clinically and molecularly well-characterized L-CMD patients.
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2023Pdm3 March 29 - Abstract 102
New avenues for treatment of Facioscapulohumeral Muscular Dystrophy
Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common forms of muscular dystrophy overall. Symptoms can present during childhood up until late adulthood, with an average age at onset of 30 years; a selective pattern of skeletal muscle weakness and a wide spectrum of disease expression are commonly observed, also within the families. The pathogenic molecular mechanism is believed to reside in an aberrant expression of the DUX4 gene due to abnormal levels of hypomethylation in the D4Z4 region on chromosome 4q35. DUX4 is a double-homeobox transcription factor that is normally expressed during em-bryogenesis and activates a core set of genes involved in zygotic development; it is then silenced in most adult tissues except thymus and testis. While evidence is growing about phenotypical variability and possible dif-ferent disease courses, knowledge of pathophysiologic mechanisms underlying those differences is still far from comprehensive. As clinical trials are finally approaching also for FSHD, understanding of the interplaying factors determining disease course, phenotypic characterization of patients, and choosing appropriate outcome measures is crucial for correct selection of molecules, trials’ design and selection of endpoints. To date, there are no approved treatments for FSHD and standard of care only implies personalized physical therapy and management of motor disability. In the last years we observed the evolution of FSHD clinical trials from non-specific anabolic or anti-inflammatory/oxidant strategies, to cutting-edge molecular therapies targeting DUX4. The accepted hypothesis involving aberrant DUX4 expression in skeletal muscle has guided the research pipeline for targeted therapies, in particular treatments reducing DUX4 gene expression. Among them, Losmapimod, a p38-mitogen activated protein kinase inhibitor that has been studied in multiple fields from oncology to cardiovascular medicine, has been proposed as a novel treatment for FSHD and a phase III clinical trial is currently recruiting patients.
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3 National Center for the Medical Consequences of Spinal Cord Injury and Medical and Surgical Service, James J Peters VA Medical Center, Bronx, NY, USA
3 National Center for the Medical Consequences of Spinal Cord Injury and Medical and Surgical Service, James J Peters VA Medical Center, Bronx, NY, USA
1 School of Sport and Exercise Science, Liverpool John Moores University, UK
2 Research Department of Physiology and Aging, University of Florida, Gainesville, Florida, USA
3 National Center for the Medical Consequences of Spinal Cord Injury and Medical and Surgical Service, James J Peters VA Medical Center, Bronx, NY, USA
Mice are commonly used to investigate muscle biology and disease, but many labs have found it difficult to produce whole muscle hypertrophy without chronic overload or very long periods of training. We have established a model of muscle growth in the rat using programmed contractions in which the plantar flexors are used to resist the dorsiflexors of the ankle [1, 2]. We will present data from experiments in the rat that show a marked increase of muscle mass, showing how the acute transcriptomic response 1 hour after an exercise session changes as a muscle adapts to daily exercise over 30 days. We will also show that a similar degree of hypertrophy is achieved after 30 days with exercise every three days, and that the transcriptomic response in this case shows less change towards an ‘endurance’ expression profile. We will also present evidence from experiments using the same approach in mice, comparing the transcriptomic response of mouse muscle and rat muscle to the same protocol. In mice we see similar changes in gene expression but no increase in muscle mass. Future comparison of the transcriptomic and protein synthetic and degradative mechanisms in these models will be informative.
Figure showing the percentage difference in mass between the left (daily stimulation) and right (contralateral unstimulated control) tibialis anterior muscles in rats (circles) and mice (squares). In mice we do not observe the progressive hypertrophy that is found in the rat with identical stimulation (100Hz, 2s ON 2s OFF, 5 sets of 10 repetitions once per day with sets separated by 2.5 minutes of rest). Rat data from reference 1.
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Eur J Transl Myol. 2023 Mar 1;33(1):11279.
2023Pdm3 March 31 - Abstract 104
Pharmacological modulation of MCU in skeletal muscle
Skeletal muscle mitochondria readily accumulate Ca2+ in response to SR store-releasing stimuli thanks to the activity of the mitochondrial calcium uniporter (MCU), the highly selective channel responsible for mitochondrial Ca2+ (mitCa2+ uptake. In skeletal muscle, MCU-dependent mitCa2+ positively regulates myofiber size by impinging on PGC1α4 and IGF1-AKT/PKB pathways.1 While the genetic modulation of the MCU has been widely applied, small molecules able to increase mitCa2+ uptake are rare. Spermine and related polyamines lower the threshold of mitCa2+ uptake.2 The p38 mitogen-activated protein kinase inhibitor SB202190 modulates mitCa2+ with a mechanism independent of p38 activity.3 Several natural plant flavonoids increase MCU activity independently of their antioxidant activity.4 Agonists and antagonists of the estrogen receptor as 4,4′,4″-(4-propyl-[1 h]-pyrazole-1,3,5-triyl)trisphenol (PPT), diethylstilbestrol, and 17-β-estradiol modulate the activity of the uniporter. By using a well-established methodology based on Aequorin, a calcium-sensitive probe that emits light upon Ca2+ binding, we screened a library of 1,600 FDA-approved drugs for their ability to modulate mitCa2+ uptake in living cells. We identified Amorolfine as a positive MCU modulator.5 Amorolfine is a morpholine antifungal drug that inhibits enzymes of the fungal sterol synthesis pathway and it is indicated for the topic treatment of mycoses. Amorolfine increases mitCa2+ uptake in Hela, C2C12 cells and adult isolated myofibers without affecting cytCa2+ and mitochondrial membrane potential. In agreement with the role of MCU in triggering hypertrophy, Amorolfine increases the size of C2C12 myotubes in an MCU-dependent manner Moreover Amorolfine significantly increases the cross-sectional area of TA and EDL muscle fibers when injected for one week in TA muscles. In light of the role of mitCa2+ uptake in sustaining aerobic metabolism the positive modulation of MCU by Amorolfine increases oxygen consumption rate in flexor digitorum brevis (FDB)-isolated myofibers.5 Thus, the positive modulation of MCU by Amorolfine could be useful to sustain muscle trophsim in different conditions characterized by muscle atrophy.
1.Mammucari C, Gherardi G, Zamparo I, Raffaello A, Boncompagni S, Chemello F, Cagnin S, Braga A, Zanin S, Pallafacchina G, Zentilin L, Sandri M, De Stefani D, Protasi F, Lanfranchi G, Rizzuto R.
The mitochondrial calcium uniporter controls skeletal muscle trophism in vivo. Cell Rep. 2015. Mar 3;10(8):1269-79. doi: 10.1016/j.celrep.2015.01.056. Epub 2015 Feb 26. PMID: 25732818; PMCID: PMC4351162. [DOI] [PMC free article] [PubMed] [Google Scholar]
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A novel regulatory mechanism of the mitochondrial Ca2+ uniporter revealed by the p38 mitogen-activated protein kinase inhibitor SB202190. FASEB J. 2002. Dec;16(14):1955-7. doi: 10.1096/fj.02-0553fje. Epub 2002 Oct 4. PMID: 12368236. [DOI] [PubMed] [Google Scholar]
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Direct activation of the mitochondrial calcium uniporter by natural plant flavonoids. Biochem J. 2004. Nov 15;384(Pt 1):19-24. doi: 10.1042/BJ20040990. PMID: 15324303; PMCID: PMC1134084. [DOI] [PMC free article] [PubMed] [Google Scholar]
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Identification and functional validation of FDA-approved positive and negative modulators of the mitochondrial calcium uniporter. Cell Rep. 2021. Jun 22;35(12):109275. doi: 10.1016/j.celrep.2021. 109275. PMID: 34161774; PMCID: PMC8242467. [DOI] [PMC free article] [PubMed] [Google Scholar]
The Tensor Tympani muscle (TTM), a small muscle placed in the medial-anterior portion of the middle ear cavity, represents a subject of lively debate. Its function and activity have been investigated for decades, but still remain unclear. Aiming to collect the available knowledge regarding this structure, the authors performed a review of the literature. Particular attention was dedicated to its anatomy and physiology. It is known that the TTM reacts to different stimuli, both auditory and non-auditory. It was hypothesized its role in the middle ear reflex to protect the cochlea from high-intensity noises, in synergy with the stapedius muscle. Moreover, the activity of the TTM was demonstrated to determine a conductive hearing loss by stiffening the ossicular chain. Other triggers for TTM contraction were described, such as vocalization, swallowing and chewing. A relationship was proposed between the TTM and the tensor veli palatini, two muscles both developing form the first pharyngeal arch, and other masticatory muscles. Some other non-auditory triggers can activate the TTM, including anticipation of loud sounds, orbital air jet and tactile stimulation of the face. Several theories regarding the function of TTM are still being postulated. Its neural connection with the brain and other muscles are still object of study. Its relationship with the eustachian tube could provide explanation to different pathological processes. Indeed, the function and activity of TTM have been speculated for decades, and nowadays it is not possible to state a definitive answer to its physiological role.
1.Fournier P, Paquette S, Paleressompoulle D, Paolino F, Devèze A, Noreña A.
Contraction of the stapedius and tensor tympani muscles explored by tympanometry and pressure measurement in the external auditory canal. Hear Res. 2022. Jul;420:108509. doi: 10.1016/j.heares.2022.108509. Epub 2022 Apr 27. PMID: 35568596. [DOI] [PubMed] [Google Scholar]
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3.Rodríguez-Vázquez JF, Sakiyama K, Abe H, Amano O, Murakami G.
Fetal Tendinous Connection Between the Tensor Tympani and Tensor Veli Palatini Muscles: A Single Digastric Muscle Acting for Morphogenesis of the Cranial Base. Anat Rec (Hoboken). 2016. Apr;299(4):474-83. doi: 10.1002/ar.23310. Epub 2016 Jan 27. PMID: 26744237 [DOI] [PubMed] [Google Scholar]
Eur J Transl Myol. 2023 Mar 1;33(1):11279.
2023Pdm3 March 31 - Abstract 61
Fascia Lata alterations in hip osteoarthritis: An observational cross-sectional study
The present study compares the structure and composition of fascia lata in healthy subjects and in patients with hip osteoarthritis (OA), to evaluate any differences in the amount of Collagen type I, Collagen type III, and Hyaluronan. Fascia lata samples from voluntary healthy subjects and patients with OA were harvested during surgery. Collagen type I (COL I), III (COL III) antibody, and biotinylated hyaluronan binding protein (HABP) immunohistochemistry stainings were used to evaluate fascial morphology and COL I, COL III, and Hyaluronan (HA) content in both groups. Ten samples from healthy subjects (group A) and 11 samples from OA patients (group B) were collected. COL I was significantly more abundant in the OA group (p = 0.0015), with a median percentage positivity of 75.2 (IQR 13.11)%, while representing only 67 (IQR: 8.71)% in control cases. COL III, with median values of 9.5 (IQR 3.63)% (OA group) and 17.10 (IQR 11)% (control cases), respectively, showed significant reduction in OA patients (p = 0.002). HA showed a median value of 10.01 (IQR 8.11)% in OA patients, denoting significant decrease (p < 0.0001) with respect to the control group median 39.31 (IQR 5.62)%. The observed differences suggest a relationship between fascial pathology and hip OA. The observed increase in COL I in OA patients, along with the reduction of COL III and HA, could lead to fascial stiffening, which could alter fascial mechanics and be linked to the development and symptoms of OA.
Boxplot comparing the percentage antibody positivity for Collagen I, Collagen III and HABP.
Key Words: Fascia, hip osteoarthritis, hyaluronan, collagen, stiffness, myofascial pain
References
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Eur J Transl Myol. 2023 Mar 1;33(1):11279.
2023Pdm3 March 31 - Abstract 76
Peculiarities of the chewing muscles electrophysiological activity in mouth breathing individuals
Various factors, that play significant role in development of facial, bony structures, formation of normal growth and functionally correct dentition, have become the subject of increasing interest recently. According to the latest studies, neuromuscular balance is considered to be the main prerequisite for preventing relapse after orthodontic treatment and also the way to optimize its outcome. One of the main factors for normal growth of the jaws is not only masticatory muscles proper, coordinated work, but also its contractility (and therefore excitability) - physiological characteristics. It should be noted, that as a result of decreased muscle activity, significant changes in the location, size and growth of the jaws can develop, which can be manifested by the vertical growth of the face. The study was conducted on the group of 65 male and female volunteers. Several breathing tests were carried out to determine the breathing type. Cephalometric analysis was performed for all individuals to conclude the position, growth type and size of the jaws. In order to reduce the dentoalveolar proprioceptive signal, all subjects had been indicated to clench on the cotton rolls and the data was obtained during maximal voluntary contraction. In mouth breathing individuals, mean electromyographic activity of both masseter and temporalis muscles registered during maximal contraction, turned out to be inhomogeneous and asymmetric, occlusal anomalies had been noted, most often - skeletal second class.
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Eur J Transl Myol. 2023 Mar 1;33(1):11279.
2023Pdm3 March 31 - Abstract 106
Craniomandibular dysfunctions – modern diagnostic methods
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Eur J Transl Myol. 2023 Mar 1;33(1):11279.
2023Pdm3 April 1 - Abstract 83
C-Terminal Agrin Fragment as a biomarker of muscle wasting and weakness in aging and disuse
2 Blau Laboratory, Stanford School of Medicine, Stanford, CA, USA
3 Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA
1 Department of Surgery, Oncology, and Gastroenterology, University of Padova, Padova, Italy
2 Blau Laboratory, Stanford School of Medicine, Stanford, CA, USA
3 Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA
4 Department of Biomedical Sciences, University of Padova, Padua, Italy.
5 CAST, Center for Advanced Studies and Technology; University G D'Annunzio of Chieti-Pescara, Chieti, Italy
6 Sapienza University of Rome, Italy
7 Ludwig Boltzmann Institute for Rehabilitation Research, Wien, Austria
8 CIR-MYO Myology Center, University of Padova, Padova, Italy
In the last decades, the extended human longevity resulted in increasing numbers of senior individuals in the general population. Ageing is accompanied by a progressive decline in muscle mass and function. It is associated with increased risk of adverse outcomes including knee or hip injuries and degeneration, falls, or bone fractures, possibly determining the onset of a clinical syndrome termed sarcopenia. Sarcopenia is not only caused by ageing (primary sarcopenia) but may be linked to the presence of several co-morbidities (secondary sarcopenia), such as disuse/inactivity, advanced organ failure, or inadequate intake of energy/proteins. Denervation and NMJ impairment have been proposed as key determinants of age-related muscle wasting and weakness. Thus, screening, monitoring and prevention of those conditions inducing muscle dysfunction is essential to improve the quality of life, potentially reducing ageing and sarcopenia-related social and economic costs. To this aim, the reliability and accessibility of non-invasive blood derived biomarkers is being evaluated. C-terminal Agrin Fragment (CAF), a circulating C-22 kDa peptide resulting from the proteolytic cleavage of agrin, a protein responsible for the neuromuscular junction (NMJ) assembly and maintenance, has been widely investigated by us and numerous other groups as circulating NMJ-related biomarker of muscle dysfunction. Essentially, serum CAF concentration was observed to increase with age and in sarcopenic individuals when compared to age-matched, medically stable peers. Serum CAF was reported also to raise following chronic inactivity or disuse and seemed to be lowered or maintained by exercise training. Finally, CAF was found to correlate with appendicular lean mass, handgrip and gait speed. Therefore, CAF seems to be a specific biomarker for screening and monitoring muscle wasting and weakness. It may be a useful tool for tailored approaches of muscle rehabilitation and for prevention or rescue of muscle dysfunction. When findings will be confirmed on larger cohort of subjects, future guidelines may be implemented for introducing CAF as a biomarker in clinical settings.
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