Laura Pedraza, Olga Laosa, Rocío Segovia-Moreno, Álvaro Alcalá, María Isabel Tornero-López, Germán Corral-Muñoz, Patricia López, Jose Antonio Carnicero, Maria Ramirez, Maria Camprubi, Leocadio Rodríguez-Mañas
{"title":"Long-term clinical, nutritional, and functional outcomes of COVID-19 patients after hospital discharge","authors":"Laura Pedraza, Olga Laosa, Rocío Segovia-Moreno, Álvaro Alcalá, María Isabel Tornero-López, Germán Corral-Muñoz, Patricia López, Jose Antonio Carnicero, Maria Ramirez, Maria Camprubi, Leocadio Rodríguez-Mañas","doi":"10.1002/rco2.97","DOIUrl":"https://doi.org/10.1002/rco2.97","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Long-term nutritional and functional status after hospitalization due to COVID-19 has been poorly described. We show the physical and nutritional stata and the symptoms compatible with Long-COVID in patients who survived after an episode of hospitalization due to COVID-19 and the associated factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Single-center prospective observational study. Clinical, nutritional, and physical function data were assessed in 345 subjects over 18 years of age hospitalized in an university hospital for a diagnosis of COVID-19 in 2020 at three different times of follow-up: 6 (<i>n</i> = 118), 9 (<i>n</i> = 115), and 15 months (<i>n</i> = 112) after discharge. All survivors discharged during each of those periods were called consecutively at the times of follow-up in order to collect data about their nutritional and functional stata, and long-COVID symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The mean age of the 345 subjects included in the present study was 62.8 years (<i>SD</i> 15.8), and 180 (52.2%) were men. The mean number of comorbidities was 2.6 (<i>SD</i> 2.1). After a mean follow-up time of 10.2 ± 3.2 months, mean Barthel score showed a decrease of 2.00 (<i>SD</i> 0.12) points, that showed to be consistent disregarding the time after discharge (6 months: 1.71 ± 4.8; 9 months: 2.17 ± 5.97; 15 months: 2.20 ± 5.25). The risk factors associated with worsening in the Barthel index score were basal Barthel index [BI < 95; odds ratio (OR): 3.34, 95% confidence interval (CI): 1.26–8.85], age (OR: 1.03, CI: 1.00–1.06, per year), having comorbidities (≥3 pathologies) (OR: 1.98, CI: 1.00–3.90), and female sex (OR: 2.68, CI: 1.47–4.90). Self-reported Long-COVID symptoms were frequent, mainly those related to functioning: fatigue/tiredness (39.4%), decreased mobility (16.2%), and subjective loss of muscle mass/strength (15.9%) plus mental complaints (depression/anxiety; 20.6%). Decreased mobility (OR 7.82, CI: 3.69–16.55), cognitive impairment (OR 6.76, CI: 2.22–20.58) and a score in SARC-F ≥ 2 (OR: 3.89; CI: 2.03–7.49) at follow-up were associated to the worsening in BI. BMI showed a modest, non-significant decrease at 6 months (−0.3 ± 1.7 kg/m<sup>2</sup>), that was fully recovered in the longest follow-up period (+0.4 ± 2.1).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Admission for COVID-19 produces a significant functional loose, mainly in those who are older, female, and with a poor basal functional status and comorbidities. This impairment does not recover sp","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"99-106"},"PeriodicalIF":0.0,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.97","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187059","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}
Kristoffer N.D. Huitfeldt Sola, Helena M. Genberg, Carla M. Avesani, Torkel B. Brismar
{"title":"Myosteatosis and not low muscle mass is associated with lower survival in kidney transplant recipients","authors":"Kristoffer N.D. Huitfeldt Sola, Helena M. Genberg, Carla M. Avesani, Torkel B. Brismar","doi":"10.1002/rco2.96","DOIUrl":"https://doi.org/10.1002/rco2.96","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Myosteatosis, that is muscle fat infiltration, is an important marker of muscle quality, affecting quality of life and survival in patients with chronic kidney disease (CKD). However, the connection between myosteatosis, skeletal muscle index (SMI) and survival in kidney transplant (KTx) recipients remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective observational study included a cohort of consecutive adult kidney recipients transplanted between 2010 and 2017 in Stockholm. Preoperative abdominal computed tomography (CT) images obtained after diagnosis of CKD 5 and within 36 months of transplantation were collected. Using established criteria, we measured muscle area at the third lumbar vertebra (L3 level) and identified low attenuation muscle, indicating myosteatosis. Each area was divided by height squared providing the SMI, and fatty muscle index (FMI). Given that there is no commonly accepted definition of sarcopenia, two cut-offs for SMI were used to define low muscle mass, Cut-off 1 (≤32.8 for women and ≤44.7 for men) and Cut-off 2 (≤38.5 for women and ≤52.4 for men). Average radiodensity of skeletal muscle and Charlson comorbidity index were calculated for each patient. The influence on survival from SMI, FMI, SMI/FMI ratio, and radiodensity was analysed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Out of 582 KTx recipients, 266 (46%) had a pre-transplant abdominal CT available. Applying SMI Cut-off 1, 30 recipients (11%) had sarcopenia compared with 106 (40%) with Cut-off 2. Neither SMI nor FMI was associated with survival. Yet there was an association between SMI/FMI ratio and survival, patients with the lowest quintile SMI/FMI ratio having a significantly lower survival when compared with the highest quintile, both in the crude model and when adjusted for age, gender, and comorbidity. Additionally, FMI, radiodensity, and SMI/FMI, but not SMI, were significantly associated with Charlson comorbidity index (<i>P</i> < 0.01).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The SMI/FMI ratio may be associated with both pre-transplant comorbidity and post-transplant survival even though the significance of SMI is unclear. This suggests that SMI/FMI ratio is a better indicator of muscular impairment than skeletal muscle quantity alone. The finding may reflect the complex interplay between muscle mass, muscular fat infiltration and metabolic health, all important determinants of wellness and longevity. In summary, our study underscores the potential of the SMI/FMI ratio a","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"91-98"},"PeriodicalIF":0.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.96","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187337","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}
Nadège Zanou, Vincent Gremeaux, Nicolas Place, Romuald Lepers
{"title":"Cardiovascular and muscular plasticity in an endurance-master athlete following 12 weeks of detraining and retraining: a case study","authors":"Nadège Zanou, Vincent Gremeaux, Nicolas Place, Romuald Lepers","doi":"10.1002/rco2.93","DOIUrl":"https://doi.org/10.1002/rco2.93","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study examined the cardiorespiratory and muscular adaptations of a 53-year-old endurance master athlete following 12 weeks of detraining and retraining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data were collected before and after detraining, and after retraining. Maximal oxygen uptake (VO<sub>2max</sub>) was evaluated during maximal cycling exercise. Proteins involved in muscle contraction, mitochondrial function and glycolysis were investigated using western blot analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>VO<sub>2max</sub> decreased by 7% after detraining and was 5% greater than baseline after retraining. Detraining induced an important increase in the ryanodine receptor type 1 protein levels (RyR1, +44%) with a decrease in the protein levels of its stabilizer FKBP12 (−24%). We observed a 138% increase in the sarco-endoplasmic reticulum ATPase 1 protein and a 42% increase in the myosin heavy chain fast-twitch protein in response to detraining. This was associated with depressed levels of the mitochondrial biogenesis and oxidative phosphorylation (OXPHOS) proteins, while the expression of the mitochondrial dynamic proteins appeared stimulated. Twelve weeks of retraining reversed almost all the alterations observed in muscle proteins, but specifically increased mitochondrial biogenesis, OXPHOS and antioxidant defence proteins as well as the glucose transporter 4 (Glut-4, +36%) and hexokinase (+100%) proteins levels above the baseline. The mitochondrial dynamic proteins were further increased with the retraining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These data provide novel information on cardiorespiratory and muscular plasticity, suggesting that highly endurance-trained athletes might show substantial muscular adaptations while retrained after a detraining period and call for more extensive clinical trials.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"82-90"},"PeriodicalIF":0.0,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.93","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187332","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}
Benjamin Rush, Sujay Garlapati, Jevin Lortie, Katie Osterbauer, Timothy J. Colgan, Daiki Tamada, Toby C. Campbell, Anne Traynor, Ticiana Leal, Kenneth Lee, Scott B. Reeder, Adam J. Kuchnia
{"title":"Uncorrected and subcutaneous fat-corrected echo intensities are similarly associated with magnetic resonance imaging per cent fat","authors":"Benjamin Rush, Sujay Garlapati, Jevin Lortie, Katie Osterbauer, Timothy J. Colgan, Daiki Tamada, Toby C. Campbell, Anne Traynor, Ticiana Leal, Kenneth Lee, Scott B. Reeder, Adam J. Kuchnia","doi":"10.1002/rco2.92","DOIUrl":"https://doi.org/10.1002/rco2.92","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Establishing interchangeable biomedical imaging-based measures to assess myosteatosis clinically may lead to the prevention of muscle wasting, yet neither a consensus measure nor a conversion between measures exists. Ultrasound echo intensity (EI) potentially assesses myosteatosis, but subcutaneous adipose tissue (SAT) thickness and user force application have been shown to influence EI. Although correction factors exist to adjust EI for SAT thickness, they are modelled against poor or no reference measures. Modelling EI corrections against a robust reference measure of myosteatosis, like magnetic resonance imaging (MRI)-based proton density fat fraction (PDFF), is necessary for EI's clinical application.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Healthy young adults, healthy older adults, and older adults undergoing treatment for lung cancer (<i>n</i> = 10 per group with 50% females) had PDFF and EI at 0, 5, 10, and 15 N measured on their right rectus femoris (RF). We compared EI, SAT thickness, and RF thickness between forces and groups and assessed the relationships between EI adjusted by four different correction factors and PDFF.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The mean age of our sample was 48.63 ± 19.68 years and had a body mass index of 25.21 ± 5.19 kg/m<sup>2</sup>. The correlation between PDFF and raw EI was <i>r</i> = 0.59 (<i>P</i> < 0.001) with negligible increases by previously published correction factors (Young: 0.62, <i>P</i> < 0.001; Neto Müller: 0.61, <i>P</i> < 0.001). EI, SAT thickness, and RF thickness did not significantly differ between forces (<i>χ</i><sup>2</sup> = 0.31, <i>P</i> = 0.957; <i>χ</i><sup>2</sup> = 2.39, <i>P</i> = 0.496; and <i>χ</i><sup>2</sup> = 7.75, <i>P</i> = 0.051, respectively). EI and PDFF were significantly lower among young healthy adults compared with older adult groups (<i>χ</i><sup>2</sup> = 12.88, <i>P</i> = 0.002, and <i>χ</i><sup>2</sup> = 9.13, <i>P</i> = 0.010, respectively).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>EI is correlated with PDFF regardless of force with no improvement from previously published correction factors. Our results suggest that EI is clinically useful and influenced by fat content, yet correction factors must account for more than SAT thickness alone and require further investigation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"66-75"},"PeriodicalIF":0.0,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.92","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475098","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}
Ashok Narasimhan, Mahalakshmi Kumaran, Ioannis Gioulbasanis, Richard J.E. Skipworth, Oliver F. Bathe, Stein Kaasa, Florian Strasser, Bruno Gagnon, Vickie Baracos, Sambasivarao Damaraju
{"title":"A genome wide association study to identify germline copy number variants associated with cancer cachexia: a preliminary analysis","authors":"Ashok Narasimhan, Mahalakshmi Kumaran, Ioannis Gioulbasanis, Richard J.E. Skipworth, Oliver F. Bathe, Stein Kaasa, Florian Strasser, Bruno Gagnon, Vickie Baracos, Sambasivarao Damaraju","doi":"10.1002/rco2.91","DOIUrl":"https://doi.org/10.1002/rco2.91","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cancer cachexia is characterized by severe loss of muscle and fat involving a complex interplay of host–tumour interactions. While much emphasis has been placed on understanding the molecular mechanisms associated with cachexia, understanding the heritable component of cachexia remains less explored. The current study aims to identify copy number variants (CNV) as genetic susceptibility determinants for weight loss in patients with cancer cachexia using genome wide association study (GWAS) approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 174 age-matched patients with oesophagogastric or lung cancer were classified as weight losing (>10% weight loss) or weight stable participants (<2% weight loss). DNA was genotyped using Affymetrix SNP 6.0 arrays to profile CNVs. We tested CNVs with >5% frequency in the population for association with weight loss. Pathway analysis was performed using the genes embedded within CNVs. To understand if the CNVs in the present study are also expressed in skeletal muscle of patients with cachexia, we utilized two publicly available human gene expression datasets to infer the relevance of identified genes in the context of cachexia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the associated CNVs, 5414 CNVs had embedded protein coding genes. Of these, 1583 CNVs were present at >5% frequency. We combined multiple contiguous CNVs within the same genomic region and called them Copy Number Variable Region (CNVR). This led to identifying 896 non-redundant CNV/CNVRs, which encompassed 803 protein coding genes. Genes embedded within CNVs were enriched for several pathways implicated in cachexia and muscle wasting including JAK–STAT signalling, Oncostatin M signalling, Wnt signalling and PI3K-Akt signalling. This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. Further, we show that a subset of CNV/CNVR embedded genes identified in the current study are common with the previously published skeletal muscle gene expression datasets, indicating that expression of CNV/CNVR genes in muscle may have functional consequences in patients with cachexia. These genes include CPT1B, SPON1, LOXL1, NFAT5, RBFOX1, and PCSK6 to name a few.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. The data generated will aid in future replication studies in larger cohorts to account for genetic susceptibility to weig","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"55-65"},"PeriodicalIF":0.0,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.91","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475100","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}
Danielle A. Debruin, Jasmaine Murphy, Dean G. Campelj, Ryan Bagaric, Cara A. Timpani, Craig A. Goodman, Erik D. Hanson, Emma Rybalka, Alan Hayes
{"title":"Combined orchiectomy and limb immobilization recapitulate early age-related changes to skeletal muscle in mice","authors":"Danielle A. Debruin, Jasmaine Murphy, Dean G. Campelj, Ryan Bagaric, Cara A. Timpani, Craig A. Goodman, Erik D. Hanson, Emma Rybalka, Alan Hayes","doi":"10.1002/rco2.90","DOIUrl":"https://doi.org/10.1002/rco2.90","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Muscle mass and function decline in middle age, ultimately resulting in sarcopenia in the elderly and poor health outcomes, reducing quality of life. There is a lack of cost- and time-effective murine models that recapitulate the physiological changes associated with muscle mass decline to study possible interventions to delay sarcopenia. We aimed to evaluate the effectiveness of combining orchiectomy (ORC) surgery to simulate age-related androgen decline and hindlimb immobilization (IM) in inducing age-related skeletal muscle changes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Four-month-old male C57BL/6J mice (<i>n =</i> 10) were subjected to ORC, followed by IM (right hindlimb casting) for 14 days. Upon completion of the casting period, ex vivo muscle contractile function, histology, and various mitochondrial markers were assessed, and results were compared with age-matched controls (CON; <i>n</i> = 8) and middle-aged (MA; 12 ± 1 months, <i>n</i> = 9) animals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>IM combined with ORC induced a 30%–40% decrease in muscle mass across multiple hindlimb muscles (<i>P</i> < 0.0001), with the magnitude of muscle loss comparable with the MA group when corrected for body weight (<i>P</i> < 0.0001). In the IM limb of ORC mice, soleus muscle force significantly decreased when compared with the contralateral limb (<i>P <</i> 0.05) and aged-matched CON group (<i>P <</i> 0.05). The decrements in muscle force and mass present in the IM limb of ORC mice were accompanied by a 70% reduction in the expression of the muscle structural protein dystrophin and various mitochondrial markers, including cytochrome C (−55%), peroxisome proliferator-activated receptor gamma co-activator 1-beta (PGC1-β) (−49%), and cytochrome oxidase IV (COX-IV) (−73%) when compared with CON animals (<i>P</i> < 0.001). Lastly, our model also demonstrated specific fibre-type shifts in fast- and slow-twitch muscles, which mimicked changes in the MA group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Applying treatments during IM could target acute muscle atrophy in MA adults, while applying them following cast removal in a low-testosterone environment could represent a window for rehabilitation therapeutics.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"40-54"},"PeriodicalIF":0.0,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.90","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475099","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":"Betulinic acid ameliorates cast-immobilized skeletal muscle atrophy but not denervation-induced skeletal muscle atrophy","authors":"Yuki Enoki, Yuki Kanezaki, Isamu Takahata, Kazuaki Taguchi, Kazuaki Matsumoto","doi":"10.1002/rco2.89","DOIUrl":"https://doi.org/10.1002/rco2.89","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Terpenoids have gained attention as therapeutic agents for skeletal muscle atrophy owing to their various physiological activities. In this study, we screened four terpenoids for their therapeutic potential against muscle atrophy in cultured cells and evaluated the effectiveness of betulinic acid in two disuse muscle atrophy models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>C2C12 cells were used as the skeletal muscle model in cell culture experiments. Betulinic acid (100 mg/kg, twice daily) was administered to two different mouse models of muscle atrophy (established using the sciatic denervation and casting methods) for 7 days.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In myotube experiments, the mRNA expression of atrogin-1 and myostatin was significantly suppressed by betulinic and ursolic acids (<i>P</i> < 0.05). In the differentiation phase of C2C12 myotubes, the mRNA expression levels of myoD and myogenin were significantly increased by betulinic acid (<i>P</i> < 0.05). In addition, apelin and irisin were also significantly increased by betulinic acid (<i>P</i> < 0.05 and 0.01, respectively). Consequently, betulinic acid was administered to the aforementioned muscle atrophy models. Betulinic acid did not inhibit the decrease in skeletal muscle weight observed in the denervation model. However, it significantly inhibited the decrease in tibialis anterior (TA) and extensor digitorum longus (EDL) weights and grip strength observed in the cast-immobilized skeletal muscle atrophy model (TA: Cast + Veh vs. Cast + Bet = 42.6 ± 1.0 vs. 46.0 ± 0.8 mg, <i>P</i> < 0.01; EDL: Cast + Veh vs. Cast + Bet = 9.0 ± 0.4 vs. 11.3 ± 0.5 mg, <i>P</i> < 0.01; grip strength: Cast + Veh vs. Cast + Bet = 222 ± 4.8 vs. 245 ± 3.6 g, <i>P</i> < 0.05). In addition, betulinic acid administration partially inhibited the decrease in skeletal muscle cross-sectional area.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Betulinic acid alleviated muscle atrophy in the cast model of muscle atrophy and has therapeutic potential for the treatment of immobilized disuse skeletal muscle atrophy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"30-39"},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.89","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475087","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}
Dong-liang Yuan, Wen-qing Xie, Miao He, Deng-jie Yu, Heng-zhen Li, Hong-fu Jin, Guang Yang, Bing-zhou Ji, Wen-feng Xiao, Yu-sheng Li
{"title":"Publication trends and hot spots in the Journal of Cachexia, Sarcopenia and Muscle: A bibliometric analysis (2010–2022)","authors":"Dong-liang Yuan, Wen-qing Xie, Miao He, Deng-jie Yu, Heng-zhen Li, Hong-fu Jin, Guang Yang, Bing-zhou Ji, Wen-feng Xiao, Yu-sheng Li","doi":"10.1002/rco2.88","DOIUrl":"https://doi.org/10.1002/rco2.88","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The <i>Journal of Cachexia, Sarcopenia and Muscle</i> is a quarterly peer-reviewed medical journal published by WILEY since 2010 and has been dedicated to advancing research on chronic diseases, especially cachexia and sarcopenia. Over the past 12 years, sarcopenia research worldwide has significantly changed. This study aimed to investigate different aspects of studies published in this journal.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using the term ‘Journal of Cachexia, Sarcopenia and Muscle’, we retrieved related publications from the Web of Science and PubMed databases. Studies published in this journal were classified and analysed from different perspectives, such as the number of studies, total citations, times cited per item, H-index, research area, article types, institutions, country and funding agency. The VOS viewer software was used for co-occurrence, bibliographic coupling, co-citation and co-authorship analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From 2010 to 2022, 1194 studies were published in the <i>Journal of Cachexia, Sarcopenia and Muscle</i>. The United States was the highest contributor, with the most publications and citations and the highest H-index. Italy ranked first for the times cited per item. The main research area was geriatrics and gerontology. von Haehling S was the author with the highest impact. The National Institutes of Health, USA, and the United States Department of Health Human Services funded the maximum number of studies. The top 5 most frequently used keywords in all publications over 12 years were sarcopenia, cachexia, skeletal muscle, body composition and muscle mass. The <i>Journal of Cachexia, Sarcopenia and Muscle</i> was cited the most by <i>Nutrients</i>, and PLOS ONE was cited the most by the <i>Journal of Cachexia, Sarcopenia and Muscle</i>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Publications in the <i>Journal of Cachexia, Sarcopenia and Muscle</i> have significantly increased from 2010 to 2022, especially in recent years. The United States is still the leader in sarcopenia research. Future submissions to this journal will continue to focus on sarcopenia, cachexia, skeletal muscle, body-composition and muscle mass. The aetiology, molecular mechanisms and outcomes of sarcopenia and cachexia are current research hotspots.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"17-29"},"PeriodicalIF":0.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.88","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141453593","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":"Hypoxia-inducible factor prolyl hydroxylase domain inhibitors may mitigate loss of skeletal muscle mass in haemodialysis patients","authors":"Hiroko Hashimoto, Shintaro Mandai, Satomi Shikuma, Mai Kimura, Hayato Toma, Yuki Sakaguchi, Moe Kimura, Jun Ota, Yoshihiko Chiba, Keigo Sakai, Susumu Horiuchi, Susumu Adachi, Shinichi Uchida","doi":"10.1002/rco2.87","DOIUrl":"10.1002/rco2.87","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Chronic kidney disease patients particularly with renal anaemia hyporesponsive to erythropoiesis-stimulating agents (ESAs) are at a greater risk of having skeletal muscle mass (SMM) loss. Hypoxia-inducible factor prolyl hydroxylase domain inhibitor (HIF-PHI), a novel therapeutic agent for renal anaemia, potentially promotes angiogenesis, muscle repair, and homeostasis. However, effects of HIF-PHIs on SMM remain unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective observational cohort study enrolled 292 Japanese adults receiving maintenance haemodialysis at our dialysis centre. The dataset included 11 patients who received daprodustat for 6 months or longer during 1 December 2020 through 30 June 2022. From the previously published pooled cohort, we enrolled 281 participants from 1 August 2018 to 31 July 2019 prior to the approval of HIF-PHIs for renal anaemia. SMM was assessed using modified creatinine index (mg/kg/day) calculated by age, sex, serum creatinine, and single-pool <i>Kt</i>/<i>V</i>. Annual changes of SMM [ΔSMM (%)] were analysed with the least squares regression model and mixed-effects model during 6- to 12-month follow-up period.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The median age of the participants was 63 years [interquartile range (IQR), 54–71 years], and 33% were female. The median ΔSMM levels (IQR) in the least squares regression model were 4.0% (−1.7% to 9.3%) in the HIF-PHI group, 0.20% (−2.1% to 2.1%) in the no ESA group, and −0.94% (−3.0% to 1.3%) in the high ESA group using darbepoetin equivalent to 20 μg or more per week. Those in the mixed-effects model were −1.7% (−1.2% to 3.8%), 0.09% (−1.4% to 1.3%), and −0.74% (−2.0% to 0.8%), respectively. The multivariable linear regression models revealed that HIF-PHI use was associated with greater ΔSMM compared with the high ESA group [coefficient, 3.737; 95% confidence interval (CI), 1.216–6.258 in the least squares regression model or coefficient, 1.635; 95% CI, 0.068–3.201 in the mixed-effects model, respectively].</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>HIF-PHI use led to greater ΔSMM in maintenance haemodialysis patients. HIF-PHIs may minimize loss of SMM in patients with end-stage kidney disease and renal anaemia.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"6-16"},"PeriodicalIF":0.0,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.87","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139387110","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}