Role of peripheral muscle function in rehabilitation

2005 ◽  
pp. 80-90
Author(s):  
Didier Saey ◽  
François Maltais
Keyword(s):  
Muscle Function ◽  
Peripheral Muscle

scholarly journals The role of the oral myologist with orthognathic surgery -- A patient/therapist's point of view

1986 ◽  
Vol 12 (2) ◽  
pp. 13-14
Author(s):  
Joy Moeller
Keyword(s):  
Surgical Treatment ◽  
Muscle Function ◽  
Orthognathic Surgery ◽  
Muscle Fibers ◽  
Point Of View ◽  
Short Time

Introduction: The trauma of orthognathic surgery on muscle function has frequently been overlooked by oral surgeons. The attitude of many surgeons is that the muscle fibers will adapt to the new structure in a short time. The purpose of this paper is to dispute this attitude and to address the need for the oral rnyologist to assume an important role in the healing and post-surgical treatment of the patient.

scholarly journals miR-206 family is important for mitochondrial and muscle function, but not essential for myogenesis in vitro

2019 ◽  
Author(s):  
Roza K. Przanowska ◽  
Ewelina Sobierajska ◽  
Zhangli Su ◽  
Kate Jensen ◽  
Piotr Przanowski ◽  
...  
Keyword(s):  
Muscle Function ◽  
Skeletal Muscle Regeneration ◽  
C2c12 Myoblasts ◽  
Skeletal Myoblasts ◽  
Microrna Targets ◽  
Microrna Family ◽  
Differentiation Pathways

AbstractmiR-206, miR-1a-1 and miR-1a-2 are induced during differentiation of skeletal myoblasts and promote myogenesis in vitro. miR-206 is required for skeletal muscle regeneration in vivo. Although this microRNA family is hypothesized to play an essential role in differentiation, a triple knockout of the three genes has not been done to test this hypothesis. We report that triple KO C2C12 myoblasts generated using CRISPR/Cas9 method differentiate despite the expected de-repression of the microRNA targets. Surprisingly, their mitochondrial function is diminished. Triple KO mice demonstrate partial embryonic lethality, most likely due to the role of miR-1a in cardiac muscle differentiation. Two triple KO mice survive and grow normally to adulthood with smaller myofiber diameter and diminished physical performance. Thus, unlike other microRNAs important in other differentiation pathways, the miR-206 family is not absolutely essential for myogenesis and is instead a modulator of optimal differentiation of skeletal myoblasts.

scholarly journals Stem Cell-Derived Exosomes Ameliorate Doxorubicin-Induced Muscle Toxicity through Counteracting Pyroptosis

2020 ◽  
Vol 13 (12) ◽  
pp. 450
Author(s):  
Fatima Bianca A. Dessouki ◽  
Rakesh C. Kukreja ◽  
Dinender K. Singla
Keyword(s):  
Muscle Function ◽  
Muscular Atrophy ◽  
Embryonic Stem ◽  
Mouse Embryonic Fibroblast ◽  
Negative Control ◽  
M1 Macrophages ◽  
Tnf Α ◽  
Embryonic Fibroblast ◽  
Muscle Toxicity

Doxorubicin (Dox)-induced muscle toxicity (DIMT) is a common occurrence in cancer patients; however, the cause of its development and progression is not established. We tested whether inflammation-triggered cell death, “pyroptosis” plays a role in DIMT. We also examined the potential role of exosomes derived from embryonic stem cells (ES-Exos) in attenuating DIMT. C57BL/6J mice (10 ± 2 wks age) underwent the following treatments: Control (saline), Dox, Dox+ES-Exos, and Dox+MEF-Exos (mouse-embryonic fibroblast-derived exosomes, negative control). Our results demonstrated that Dox significantly reduced muscle function in mice, which was associated with a significant increase in NLRP3 inflammasome and initiation marker TLR4 as compared with controls. Pyroptosis activator, ASC, was significantly increased compared to controls with an upregulation of specific markers (caspase-1, IL-1β, and IL-18). Treatment with ES-Exos but not MEF-Exos showed a significant reduction in inflammasome and pyroptosis along with improved muscle function. Additionally, we detected a significant increase in pro-inflammatory cytokines (TNF-α and IL-6) and inflammatory M1 macrophages in Dox-treated animals. Treatment with ES-Exos decreased M1 macrophages and upregulated anti-inflammatory M2 macrophages. Furthermore, ES-Exos showed a significant reduction in muscular atrophy and fibrosis. In conclusion, these results suggest that DIMT is mediated through inflammation and pyroptosis, which is attenuated following treatment with ES-Exos.

Corticosteroids and skeletal muscle function in cystic fibrosis

2003 ◽  
Vol 95 (4) ◽  
pp. 1379-1384 ◽  
Author(s):  
Sinead C. Barry ◽  
Charles G. Gallagher
Keyword(s):  
Skeletal Muscle ◽  
Cystic Fibrosis ◽  
Muscle Strength ◽  
Muscle Weakness ◽  
Muscle Function ◽  
Knee Extensor ◽  
Skeletal Muscle Function ◽  
Peripheral Muscle ◽  
Causative Effect ◽  
Concomitant Medications

Patients with cystic fibrosis (CF) have reduced peripheral muscle strength. We tested the hypothesis that steroid treatment contributes to muscle weakness in adults with CF. Twenty-three stable CF patients were studied. Measurements included knee extensor (KE), knee flexor (KF), elbow flexor (EF), handgrip (HG), expiratory (Pemax), and inspiratory (Pimax) muscle strengths. Spirometry, body mass index (BMI), and days spent in hospital over the preceding 12 mo (DH) were also measured. Average daily dose of prednisolone over the preceding 12 mo (ADD) was 5.1 mg/day. Pearson's correlation analysis revealed that ADD correlated significantly with skeletal muscle strengths (KF%, r = -0.63, P < 0.01) with the exception of HG%. These findings are independent of age, BMI, pulmonary function, and DH. Multiple-regression analysis revealed that ADD was the most significant predictor of all measures of skeletal muscle function except HG%. It was independently responsible for 54% of the variance in Pimax%, for 46% of the variance in Pemax%, for 45% of the variance in KE%, for 39% of the variance in KF%, and for 41% of the variance in EF%. Concomitant medications (e.g., theophylline) were shown to have no causative effect. Corticosteroids contribute to the skeletal muscle weakness seen in CF patients. The correlation of proximal muscle strength, but not HG strength, with steroid dosage further supports a cause-effect relationship.

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