scholarly journals Acute Muscle Trauma due to Overexercise in an Otherwise Healthy Patient with Cystic Fibrosis

2012 ◽  
Vol 2012 ◽  
pp. 1-4
Author(s):  
Henning Neubauer ◽  
Clemens Wirth ◽  
Katharina Ruf ◽  
Helge Hebestreit ◽  
Meinrad Beer
Keyword(s):  
Cystic Fibrosis ◽  
Muscle Injury ◽  
Acute Exercise ◽  
Clinical Laboratory ◽  
Well Being ◽  
Cftr Gene ◽  
Deficient Animal ◽  
Imaging Characteristics ◽  
Muscle Trauma ◽  
Exercise Induced

Cystic fibrosis (CF) is one of the most common inherited diseases and is caused by mutations in the CFTR gene. Although the pulmonary and gastrointestinal manifestations of the disease remain in the focus of treatment, recent studies have shown expression of the CFTR gene product in skeletal muscle cells and observed altered intramuscular Ca2+release dynamics in CFTR-deficient animal models. Physical exercise is beneficial for maintaining fitness and well-being in CF patients and constitutes one aspect of modern multimodal treatment, which has considerably increased life span and reduced morbidity. We report on a case of acute muscle trauma resulting from excessive dumbbell exercise in a young adult with cystic fibrosis and describe clinical, laboratory and imaging characteristics of acute exercise-induced muscle injury.

ACUTE EXERCISE-INDUCED MUSCLE INJURY

2012 ◽  
Vol 29 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Andrew McKune ◽  
Stuart Semple ◽  
Edith Peters-Futre
Keyword(s):  
Muscle Injury ◽  
Acute Exercise ◽  
Exercise Induced

scholarly journals The regulation of autophagy during exercise in skeletal muscle

2016 ◽  
Vol 120 (6) ◽  
pp. 664-673 ◽  
Author(s):  
Anna Vainshtein ◽  
David A. Hood
Keyword(s):  
Posttranslational Modifications ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Acute Exercise ◽  
Well Being ◽  
Long Term Potentiation ◽  
Peroxisome Proliferator ◽  
Chronic Exercise ◽  
Recent Developments ◽  
Exercise Induced

The merits of exercise on muscle health and well-being are numerous and well documented. However, the mechanisms underlying the robust adaptations induced by exercise, particularly on mitochondria, are less clear and much sought after. Recently, an evolutionary conserved cellular recycling mechanism known as autophagy has been implicated in the adaptations to acute and chronic exercise. A basal level of autophagy is constantly ongoing in cells and tissues, ensuring cellular clearance and energy homeostasis. This pathway can be further induced, as a survival mechanism, by cellular perturbations, such as energetic imbalance and oxidative stress. During exercise, a biphasic autophagy response is mobilized, leading to both an acute induction and a long-term potentiation of the process. Posttranslational modifications arising from upstream signaling cascades induce an acute autophagic response during a single bout of exercise by mobilizing core autophagy machinery. A transcriptional program involving the regulators Forkhead box O, transcription factor EB, p53, and peroxisome proliferator coactivator-1α is also induced to fuel sustained increases in autophagic capacity. Autophagy has also been documented to mediate chronic exercise-induced metabolic benefits, and animal models in which autophagy is perturbed do not adapt to exercise to the same extent. In this review, we discuss recent developments in the field of autophagy and exercise. We specifically highlight the molecular mechanisms activated during acute exercise that lead to a prolonged adaptive response.

scholarly journals Impact of exercise on older adults’ mood is moderated by sleep and mediated by altered brain connectivity

2020 ◽  
Vol 15 (11) ◽  
pp. 1238-1251
Author(s):  
Alfonso J Alfini ◽  
Junyeon Won ◽  
Lauren R Weiss ◽  
Casandra C Nyhuis ◽  
Alexander J Shackman ◽  
...  
Keyword(s):  
Older Adults ◽  
Aerobic Exercise ◽  
Sleep Disturbance ◽  
Acute Exercise ◽  
Well Being ◽  
Moderate Intensity ◽  
Increased Risk ◽  
Wrist Actigraphy ◽  
Exercise Induced ◽  
The Impact

Abstract Older adults comprise the fastest growing global demographic and are at increased risk of poor mental health outcomes. Although aerobic exercise and sleep are critical to the preservation of emotional well-being, few studies have examined their combined mood-enhancing effects, or the potential neural mechanisms underlying these effects. Here, we used a randomized crossover design to test the impact of acute exercise on mood and the intrinsic functional connectivity (iFC) of the cingulo-opercular network in physically healthy older adults. Wrist actigraphy provided objective indices of sleep. Results revealed that 30 min of moderate-intensity aerobic exercise acutely enhanced positive affect (PA) and reduced iFC between the cingulo-opercular network and the hippocampus. Both effects were magnified among older adults with greater sleep disturbance. Exercise-induced changes in hippocampal iFC mediated relations between sleep disturbance and exercise-induced increases in PA. These findings provide evidence that aerobic exercise enhances mood, that it does so by altering connectivity between the anterior insula—a key hub in the cingulo-opercular network—and the hippocampus and that lower sleep quality is a stronger predictor of these effects among older adults. These observations underscore the benefits of moderate-intensity exercise—a safe and scalable behavioral intervention—and provide new clues about the neural circuitry underlying the interactive effects of sleep and exercise on mood.

Acute-Exercise-Induced Alterations in Calpain and Calpastatin Expression in Rat Muscle

2009 ◽  
Vol 18 (2) ◽  
pp. 213-228 ◽  
Author(s):  
Lijing Wang ◽  
Ligong Duan ◽  
Xukun Li ◽  
Guoping Li
Keyword(s):  
Protein Expression ◽  
Muscle Injury ◽  
Acute Exercise ◽  
Muscle Protein ◽  
Exhaustive Exercise ◽  
Control Group ◽  
Calpain Activity ◽  
Protective Function ◽  
Type Method ◽  
Exercise Induced

Context:Calpains and calpastatin can degrade muscle proteins, but no research has investigated the expression pattern of calpains and calpastatin after exhaustive exercise.Objective:To investigate the alterations in expression of μ-, m-, and n-calpain and calpastatin after exhaustive exercise and its association with muscle injury.Method:64 rats divided into 2 groups, a nonexercise control group and an acute-exhaustive-exercise (AEE) group. Biopsies in the AEE group were taken at different times after exercise.Results:Calpastatin protein expression and m-calpain activity increased early after exercise, but both n-calpain protein expression and μ-calpain activity generally decreased with time. n-Calpain mRNA expression was down- regulated from late after exercise.Conclusions:The increased m-calpain activity might promote muscle-protein degradation and muscle injury. On the contrary, calpastatin might execute a protective function against muscle injury. The change in p-calpain activity was found earlier than muscle injury and therefore might serve as a useful predictor of muscle injury.

scholarly journals CFTR Cooperative Cis-Regulatory Elements in Intestinal Cells

2021 ◽  
Vol 22 (5) ◽  
pp. 2599
Author(s):  
Mégane Collobert ◽  
Ozvan Bocher ◽  
Anaïs Le Nabec ◽  
Emmanuelle Génin ◽  
Claude Férec ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cystic Fibrosis ◽  
Gene Regulation ◽  
Genetic Diseases ◽  
Regulatory Elements ◽  
Cftr Gene ◽  
Intestinal Cells ◽  
Cooperative Effects ◽  
Cis Acting ◽  
Study Techniques

About 8% of the human genome is covered with candidate cis-regulatory elements (cCREs). Disruptions of CREs, described as “cis-ruptions” have been identified as being involved in various genetic diseases. Thanks to the development of chromatin conformation study techniques, several long-range cystic fibrosis transmembrane conductance regulator (CFTR) regulatory elements were identified, but the regulatory mechanisms of the CFTR gene have yet to be fully elucidated. The aim of this work is to improve our knowledge of the CFTR gene regulation, and to identity factors that could impact the CFTR gene expression, and potentially account for the variability of the clinical presentation of cystic fibrosis as well as CFTR-related disorders. Here, we apply the robust GWAS3D score to determine which of the CFTR introns could be involved in gene regulation. This approach highlights four particular CFTR introns of interest. Using reporter gene constructs in intestinal cells, we show that two new introns display strong cooperative effects in intestinal cells. Chromatin immunoprecipitation analyses further demonstrate fixation of transcription factors network. These results provide new insights into our understanding of the CFTR gene regulation and allow us to suggest a 3D CFTR locus structure in intestinal cells. A better understand of regulation mechanisms of the CFTR gene could elucidate cases of patients where the phenotype is not yet explained by the genotype. This would thus help in better diagnosis and therefore better management. These cis-acting regions may be a therapeutic challenge that could lead to the development of specific molecules capable of modulating gene expression in the future.

Psychosocial well-being and quality of life in siblings of children with congenital heart disease: A systematic review

2021 ◽  
pp. 136749352110129
Author(s):  
Alice S Schamong ◽  
Hannah Liebermann-Jordanidis ◽  
Konrad Brockmeier ◽  
Elisabeth Sticker ◽  
Elke Kalbe
Keyword(s):  
Quality Of Life ◽  
Cystic Fibrosis ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Associated Factors ◽  
Congenital Heart ◽  
Negative Impact ◽  
Well Being

Congenital heart disease (CHD) is a major global health problem. Until recently, the siblings of this group did not receive much attention. This review, conducted from November 2019 to October 2020, aims to summarize knowledge about psychosocial well-being and quality of life (QoL), associated factors, and interventions for siblings of children with CHD. Systematic searches were conducted in PubMed, PsycINFO, PsycARTICLES, Web of Science via EBSCOhost, and CENTRAL. Twelve articles were included. Results showed that psychosocial well-being was impaired in 14% to 40% of siblings. Negative impact of illness was highest for CHD siblings compared to siblings of children with cancer, cystic fibrosis, or diabetes. QoL was impaired in up to one-third. Siblings of children with CHD and cancer rated their QoL lower than those of siblings of children with cystic fibrosis or type-1 diabetes. Associated factors were sibling age, gender, socioeconomic status, miscarriage, previous sibling death, visibility of illness, and severity of condition. Only one of two interventions focused on siblings of CHD children. Although data are scarce and inhomogeneous, it indicates that siblings of CHD children suffer from lower psychosocial well-being and QoL than siblings of children with other chronic conditions. Interventions to improve their situation should be developed.

scholarly journals A Peptide-Nucleic Acid Targeting miR-335-5p Enhances Expression of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Gene with the Possible Involvement of the CFTR Scaffolding Protein NHERF1

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 117
Author(s):  
Anna Tamanini ◽  
Enrica Fabbri ◽  
Tiziana Jakova ◽  
Jessica Gasparello ◽  
Alex Manicardi ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Nucleic Acid ◽  
Peptide Nucleic Acid ◽  
Stop Codon ◽  
Scaffolding Protein ◽  
Cftr Gene ◽  
Scaffolding Proteins ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Cystic Fibrosis Transmembrane

(1) Background: Up-regulation of the Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR) might be of great relevance for the development of therapeutic protocols for cystic fibrosis (CF). MicroRNAs are deeply involved in the regulation of CFTR and scaffolding proteins (such as NHERF1, NHERF2 and Ezrin). (2) Methods: Content of miRNAs and mRNAs was analyzed by RT-qPCR, while the CFTR and NHERF1 production was analyzed by Western blotting. (3) Results: The results here described show that the CFTR scaffolding protein NHERF1 can be up-regulated in bronchial epithelial Calu-3 cells by a peptide-nucleic acid (PNA) targeting miR-335-5p, predicted to bind to the 3′-UTR sequence of the NHERF1 mRNA. Treatment of Calu-3 cells with this PNA (R8-PNA-a335) causes also up-regulation of CFTR. (4) Conclusions: We propose miR-335-5p targeting as a strategy to increase CFTR. While the efficiency of PNA-based targeting of miR-335-5p should be verified as a therapeutic strategy in CF caused by stop-codon mutation of the CFTR gene, this approach might give appreciable results in CF cells carrying other mutations impairing the processing or stability of CFTR protein, supporting its application in personalized therapy for precision medicine.

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