JCSM rapid communications最新文献

{"title":"Psoas muscle measurement as a marker of sarcopenia predicts risk of Grade 4 or 5 baseline chronic kidney disease and its progression","authors":"Davine Yang, Sameena Iqbal, K. Rafatzand, C. Scheede-Bergdahl","doi":"10.1002/rco2.63","DOIUrl":"https://doi.org/10.1002/rco2.63","url":null,"abstract":"Psoas muscle area (PMA) has recently been found to be an appropriate surrogate for whole‐body skeletal muscle mass and a measure of sarcopenia. Sarcopenia, which includes a decreased muscle mass and correlated with physical disability, morbidity, and mortality, is prevalent in and has deleterious consequences for patients with chronic kidney disease (CKD). The current study investigates the association of PMA, as a marker of sarcopenia, with baseline kidney function and CKD progression.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"182 - 193"},"PeriodicalIF":0.0,"publicationDate":"2022-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49600761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of cachexia on dietary intakes, symptoms, and quality of life in advanced cancer","authors":"K. Amano, V. Baracos, T. Morita, T. Miura, N. Mori, Ryohei Tatara, Takaomi Kessoku, A. Tokoro, Keita Tagami, Hiroyuki Otani, M. Mori, T. Taniyama, N. Nakajima, Erika Nakanishi, J. Kako, Daisuke Kiuchi, H. Ishiki, H. Matsuoka, E. Satomi, M. Miyashita","doi":"10.1002/rco2.61","DOIUrl":"https://doi.org/10.1002/rco2.61","url":null,"abstract":"The relationships between cachexia stages and the Functional Assessment of Anorexia/Cachexia Therapy Anorexia Cachexia Subscale (FAACT ACS) 12‐item, 5‐item anorexia symptoms, and 4‐item anorexia concerns have not been investigated in Asian patients with advanced cancer.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"162 - 170"},"PeriodicalIF":0.0,"publicationDate":"2022-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48780092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistance exercise training increases skeletal muscle mitochondrial respiration in chronic obstructive pulmonary disease","authors":"L. Oberholzer, Knut Sindre Mølmen, D. Hammarström, G. S. Falch, Anne‐Kristine Meinild Lundby, B. Rønnestad, S. Ellefsen, Carsten Lundby","doi":"10.1002/rco2.58","DOIUrl":"https://doi.org/10.1002/rco2.58","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is associated with skeletal muscle mitochondrial dysfunction. Resistance exercise training (RT) is a training modality with a relatively small pulmonary demand that has been suggested to increase skeletal muscle oxidative enzyme activity in COPD. Whether a shift into a more oxidative profile following RT also translates into increased mitochondrial respiratory capacity in COPD is yet to be established.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"194 - 204"},"PeriodicalIF":0.0,"publicationDate":"2022-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44331897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota–muscle/immune interactions in rhesus macaque under simulated microgravity revealed by integrated multi‐omics analysis","authors":"Peng Zhang, Libin Shao, Jie Zhang, Lu Wang, Xiangsheng Pang, Wuchen Tao, Guangyi Fan, Ling Peng, Guanghan Kan, Wenjiong Li, Xinming Liang, Xin Liu, Xiaoping Chen","doi":"10.1002/rco2.60","DOIUrl":"https://doi.org/10.1002/rco2.60","url":null,"abstract":"Long‐term exposure to microgravity during spaceflight has adverse effects on human health including muscle atrophy, impaired immune function, and alterations in gut microbiome profile. Gut microorganisms influence a wide range of host biological processes, but their interactions with skeletal muscle and the immune system under microgravity have yet to be elucidated.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"212 - 225"},"PeriodicalIF":0.0,"publicationDate":"2022-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46595937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of low‐dose metformin on pre‐frailty among middle‐aged and elderly pre‐diabetic people","authors":"Chun‐Feng Huang, M. Shiao, Tso-Yen Mao","doi":"10.1002/rco2.55","DOIUrl":"https://doi.org/10.1002/rco2.55","url":null,"abstract":"Pre‐frailty has been identified as a clinically silent mechanism pre‐disposing people to frailty. The goal of this study is to investigate the impact of low‐dose metformin on pre‐diabetic pre‐frail patients (>50 years) on skeletal muscle mass, speed of gait, handgrip power, and health‐related quality of life (HR‐QoL).","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"33 - 39"},"PeriodicalIF":0.0,"publicationDate":"2022-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46375631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lenalidomide in cancer cachexia: a randomized trial of an anticancer drug applied for anti‐cachexia","authors":"D. Blum, C. Hertler, R. Oberholzer, S. Wolf-Linder, M. Joerger, C. Driessen, F. Strasser","doi":"10.1002/rco2.54","DOIUrl":"https://doi.org/10.1002/rco2.54","url":null,"abstract":"Cancer cachexia (CC) impacts quality of life, physical function, anticancer treatment response, and survival. Inflammation is a prominent pathomechanism of CC. This small‐scale study sets out to investigate the immunomodulatory drug lenalidomide in inflammatory CC in a randomized, double‐blind, placebo‐controlled trial.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"68 - 76"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45699965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sarcopenic obesity and the risk of hospitalization or death from coronavirus disease 2019: findings from UK Biobank.","authors":"Thomas J Wilkinson, Thomas Yates, Luke A Baker, Francesco Zaccardi, Alice C Smith","doi":"10.1002/rco2.47","DOIUrl":"10.1002/rco2.47","url":null,"abstract":"<p><strong>Background: </strong>Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2. The role of skeletal muscle mass in modulating immune response is well documented. Whilst obesity is well established as a key factor in COVID-19 and outcome, no study has examined the influence of both sarcopenia (low muscle mass) and obesity, termed 'sarcopenic obesity' on the risk of severe COVID-19.</p><p><strong>Methods: </strong>This study uses data from UK Biobank. Probable sarcopenia was defined as low handgrip strength. Sarcopenic obesity was mutually exclusively defined as the presence of obesity and low muscle mass [based on two established criteria: appendicular lean mass (ALM) adjusted for either (i) height or (ii) body mass index]. Severe COVID-19 was defined by a positive severe acute respiratory syndrome coronavirus 2 test result in a hospital setting and/or death with a primary cause reported as COVID-19. Fully adjusted logistic regression models were used to analyse the associations between sarcopenic status and severe COVID-19. This work was conducted under UK Biobank Application Number 52553.</p><p><strong>Results: </strong>We analysed data from 490 301 UK Biobank participants (median age 70.0 years, 46% male); 2203 (0.4%) had severe COVID-19. Individuals with probable sarcopenia were 64% more likely to have had severe COVID-19 (odds ratio 1.638; <i>P</i> < 0.001). Obesity increased the likelihood of severe COVID-19 by 76% (<i>P</i> < 0.001). Using either ALM index or ALM/body mass index to define low muscle mass, those with sarcopenic obesity were 2.6 times more likely to have severe COVID-19 (odds ratio 2.619; <i>P</i> < 0.001). Sarcopenia alone did not increase the risk of COVID-19.</p><p><strong>Conclusions: </strong>Sarcopenic obesity may increase the risk of severe COVID-19, over that of obesity alone. The mechanisms for this are complex but could be a result of a reduction in respiratory functioning, immune response, and ability to respond to metabolic stress.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"3-9"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8441916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39432676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis.","authors":"Huibin Tang, Michael Kim, Myung Lee, Kellie Baumann, Francesca Olguin, Hao He, Yoyo Wang, Bowen Jiang, Shuhuan Fang, Jinguo Zhu, Kun Wang, Hui Xia, Yang Gao, Harrison B Konsker, Emmanuel A Fatodu, Marco Quarta, Justin Blonigan, Thomas A Rando, Joseph B Shrager","doi":"10.1002/rco2.57","DOIUrl":"10.1002/rco2.57","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Skeletal muscle mass is regulated by intracellular anabolic and catabolic activities. Increased catabolic activity can shift the balance towards net protein breakdown and muscle atrophy. Mitochondrial oxidative stress activates catabolism and is linked to muscle loss. Reducing mitochondrial oxidative stress is thus a plausible approach to prevent muscle atrophy. We tested this concept in age-dependent muscle atrophy by genetically overexpressing the mitochondrial antioxidant thioredoxin-2 (TXN2).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We tested the functional role of TXN2 using ageing (&lt;i&gt;n&lt;/i&gt; = 7-10 per group) and denervation (&lt;i&gt;n&lt;/i&gt; = 3 per group) models in a transgenic mouse line that overexpresses TXN2. We investigated if overexpression of TXN2 blocks muscle loss in these models by examination of muscle weight, fibre size, and fibre number in young (~7 months) and aged (~26 months) TXN2-transgenic mice and controls. We studied the underlying mechanisms by mRNA and protein assays including transcriptomic profiling, western blot analysis, immunostaining, as well as succinate dehydrogenase, dihydroethidium, and terminal deoxynucleotidyl transferase dUTP nick end labelling staining.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Overexpression of TXN2 did not significantly alter the baseline skeletal muscle size, weight, fibre type distribution, or expression of mitochondrial respiratory chain components, but it did preserve muscle mass during ageing. The hindlimb muscle mass in aged TXN-transgenic mice was ~21-24% greater (in tibialis anterior, gastrocnemius/soleus combined, and tibialis anterior/extensor digitorum longus combined) than in age-matched controls (all &lt;i&gt;P&lt;/i&gt; &lt; 0.05). The reduction in both muscle fibre number (872 ± 206 vs, 637 ± 256 fibres in extensor digitorum longus muscle, &lt;i&gt;P&lt;/i&gt; &lt; 0.05) and muscle fibre size (1959 ± 296 vs. 1477 ± 564 μm&lt;sup&gt;2&lt;/sup&gt; in tibialis anterior muscle, &lt;i&gt;P&lt;/i&gt; &lt; 0.05) seen in young vs. aged control muscles was not significant in young vs. aged TXN-transgenic mice (both &lt;i&gt;P&lt;/i&gt; &gt; 0.05). Transcriptomic analysis revealed that catabolic genes that are up-regulated in ageing muscle, including those subserving apoptosis and the ubiquitin-like conjugation system, were normalized by TXN2 overexpression. Further, overexpressing TXN2 suppressed oxidative stress and caspase-9/3-mediated apoptotic signalling in the aged muscle at the protein level. Although denervation and its effects have been considered a component of age-related muscle atrophy, TXN2 overexpression failed to attenuate atrophy in an acute denervation model (TXN-transgenic vs. control mice, &lt;i&gt;P&lt;/i&gt; &gt; 0.05), despite preventing denervation-induced oxidative stress and apoptosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Mitochondrial oxidative stress appears to play a crucial role in effecting chronic age-dependent, but not acute neurogenic, muscle atrophy. Increased TXN2 protects muscle against oxidative stress-associated catabolic ac","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"130-145"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11995840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43062471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Muscle wasting in cancer: opportunities and challenges for exercise in clinical cancer trials.","authors":"Ciaran M Fairman,&nbsp;Simon Lønbro,&nbsp;Thomas D Cardaci,&nbsp;Brandon N VanderVeen,&nbsp;Tormod S Nilsen,&nbsp;Angela E Murphy","doi":"10.1002/rco2.56","DOIUrl":"https://doi.org/10.1002/rco2.56","url":null,"abstract":"<p><strong>Background: </strong>Low muscle in cancer is associated with an increase in treatment-related toxicities and is a predictor of cancer-related and all-cause mortality. The mechanisms of cancer-related muscle loss are multifactorial, including anorexia, hypogonadism, anaemia, inflammation, malnutrition, and aberrations in skeletal muscle protein turnover and metabolism.</p><p><strong>Methods: </strong>In this narrative review, we summarise relevant literature to (i) review the factors influencing skeletal muscle mass regulation, (ii) provide an overview of how cancer/treatments negatively impact these, (iii) review factors beyond muscle signalling that can impact the ability to participate in and respond to an exercise intervention to counteract muscle loss in cancer, and (iv) provide perspectives on critical areas of future research.</p><p><strong>Results: </strong>Despite the well-known benefits of exercise, there remains a paucity of clinical evidence supporting the impact of exercise in cancer-related muscle loss. There are numerous challenges to reversing muscle loss with exercise in clinical cancer settings, ranging from the impact of cancer/treatments on the molecular regulation of muscle mass, to clinical challenges in responsiveness to an exercise intervention. For example, tumour-related/treatment-related factors (e.g. nausea, pain, anaemia, and neutropenia), presence of comorbidities (e.g. diabetes, arthritis, and chronic obstructive pulmonary disease), injuries, disease progression and bone metastases, concomitant medications (e.g., metformin), can negatively affect an individual's ability to exercise safely and limit subsequent adaptation.</p><p><strong>Conclusions: </strong>This review identifies numerous gaps and oppportunities in the area of low muscle and muscle loss in cancer. Collaborative efforts between preclinical and clinical researchers are imperative to both understanding the mechanisms of atrophy, and develop appropriate therapeutic interventions.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":" ","pages":"52-67"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9481195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40367778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Issue Information","authors":"","doi":"10.1002/rco2.42","DOIUrl":"https://doi.org/10.1002/rco2.42","url":null,"abstract":"No abstract is available for this article.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47497999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}