The predictice valve of combining sarcopenia and clinical muti-pramater for postoperative complications of colorectal cancer patients
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ABSTRACT:
DISEASE(S): Sarcopenia, Colorectal Cancer
PROVIDER: 88331 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Interventions: Experimental group:nutrition and exercise investigation and Intervention;Control Group:nutrition and exercise investigation
Primary outcome(s): Skeletal muscle mass and strength;Nutrition assessment;physical examination
Study Design: Case-Control study
| 47924 | ecrin-mdr-crc
Project description:AbstractBackground: A decreased intramuscular carnitine status with aging may contribute to frailty and fatigue, but studies are often confounded by sex-heterogeneity and lack of control groups. We hypothesize that muscle carnitine deficiency is associated with (pre-)frailty, diminished physical performance and altered mitochondrial function, possibly in a sex-dependent manner. This was tested in well-matched age groups, allowing gender-specific analyses. Methods: A cross-sectional study was performed in well-matched fit (n = 15) and (pre-)frail (n = 13) old males as well as in fit (n = 15) and (pre-)frail (n = 11) old females, using young males (n = 13) and females (n = 13) as healthy controls. In the elderly, frailty was assessed according to the Fried criteria and physical performance was determined by 400-m walk test, short physical performance battery and handgrip strength. Acylcarnitine status was assessed in muscle biopsies and blood plasma using liquid chromatography-tandem mass spectrometry. Muscle mitochondrial gene expression was analyzed. Results: Intramuscular total carnitine levels and short chain acylcarnitine levels were lower in (pre-)frail old females compared to fit old females and young females, whereas no differences were observed in males. Intramuscular short chain acylcarnitine levels were associated with low physical performance in females, even after correction for muscle mass (%), whereas in males no such association was found. The decline in short chain acylcarnitine levels in (pre-)frail old females was associated with low expression of genes involved in mitochondrial energy production and mitochondrial functionality. Conclusions: In (pre-)frail old females, intramuscular total carnitine levels and short chain acylcarnitine levels are decreased and this decrease is accompanied by reduced physical performance and low expression of a wide range of genes involved in mitochondrial function.
2023-02-04 | GSE144304 | GEO
Project description:Genome wide DNA methylation profiling of muscle tissue genomic DNA. The Illumina Infinium MethylationEPIC array was used to obtain DNA methylation profiles across approximately 850,000 CpGs. Samples were male, taken from both the Hertfordshire Sarcopenia Study (HSS, n=34) and the Hertfordshire Sarcoepnia Study exension (HSSe, n=44), to determine DNA methylation associations with measures of muscle mass and function. We further aimed to test whether differences in the muscle methylome are associated with sarcopenia in older individuals. We found significant associations between DNA methylation in the muscle tissue and sarcopenia, as well as individual measures of muscle mass and function, enriched around EZH2 binding sites.
2021-12-15 | GSE154980 | GEO
Project description:Abstract Background: The prevalence of sarcopenia is increasing and effective interventions are required to prevent or reverse age-related muscle loss. However it is often challenging expensive and time-consuming to develop and test the effectiveness of such interventions. Furthermore translational animal models that adequately mimic underlying physiological pathways are scarce. Strong predictors for the incidence of sarcopenia include a sedentary life-style and malnutrition. Therefore our objective was to investigate the translational value of three potential mouse models for sarcopenia namely partial immobilized caloric restricted (CR) and a combination (immobilized & CR) model. Methods: C57BL/6J mice were calorically restricted (-40%) and/or one hindleg was immobilized for two weeks to induce loss of muscle mass and function. Muscle mass function and diameter and distribution of slow (type 1) and fast ( type 2) myofibers were compared to those of young control (4 months) and old reference mice (21 months). Transcriptome analysis of quadriceps muscle was performed to identify underlying pathways and were compared with those being expressed in aged human vastus lateralis muscle-biopsies using a meta-analysis of five different human studies. Results: Caloric restriction induced overall loss of lean body mass (-15% p<0.001) whereas immobilization decreased muscle strength (-28% p<0.001) and muscle mass of hindleg muscles specifically (on average -25% p<0.001). The proportion of slow myofibers increased with aging in mice (+5% p<0.05) and this was not recapitulated by the CR and/or immobilization models. The diameter of fast myofibers decreased with aging (-7% p<0.05) and this was mimicked by all models. Transcriptome analysis revealed that the combination of CR and immobilization recapitulated more pathways characteristic for human muscle-aging (73%) than naturally aged (21 months old) mice (45%). These pathways included critical pathways relevant for protein synthesis/ breakdown (mitochondrial) metabolism neurology and the vascular system. Conclusions: The combination model exhibits loss of both muscle mass (due to CR) and function (due to immobilization) and has a remarkable similarity with pathways underlying human sarcopenia. Our results demonstrate that naturally aging up to 21 months in mice only partially recapitulates the human pathology with fewer overlapping pathways than the combination model. These findings underline that external factors such as sedentary behavior and malnutrition are key elements of a translational mouse model and favor the combination model as a rapid model for testing the treatments against sarcopenia.
2022-12-16 | GSE213148 | GEO
Project description:Similar to remote ischemic preconditioning bouts of exercise may possess immediate protective effects against ischemia-reperfusion injury. However, underlying mechanisms are largely unknown. This study compared the impact of single and repeated handgrip exercise versus remote ischemic preconditioning on inflammatory biomarkers in patients with cerebral small vessel disease (cSVD). In this crossover study, 14 patients with cSVD were included. All participants performed 4-days of handgrip exercise (4x5-minutes at 30% of maximal handgrip strength) and remote ischemic preconditioning (rIPC; 4x5-minutes cuff occlusion around the upper arm) twice daily. Patients were randomized to start with either handgrip exercise or rIPC and the two interventions were separated by >9 days. Venous blood was drawn before and after one intervention, and after 4-days of repeated exposure. We performed a targeted proteomics on inflammation markers in all blood samples.
2023-03-11 | PXD037267 | Pride
Project description:The purpose of this study was to evaluate the effect of fish oil-derived n-3 PUFA therapy, which had statistically and clinically significant beneficial effects on muscle mass and strength, on skeletal muscle gene expression profile. We selected 10 subjects with the largest hypertrophy response (change in thigh muscle volume) from the treatment group.
2016-07-01 | E-GEOD-68894 | biostudies-arrayexpress
Project description:Androgens have a strong effect against skeletal muscles to increase muscle mass and strength. However, a molecular mechanism of AR action on muscle strength is not clear. To identify the target genes of AR in skeletal muscle, we generated myofiber specific ARKO using HSA-Cre and AR flox mice (cARKO). Nine-week-old female control and cARKO mice were treated with or without DHT for 4 weeks. After euthenization, gastrocunemius muscle were collected and total RNA were extracted.
2021-03-10 | GSE152756 | GEO
Project description:Mitochondrial dysfunction caused by mitochondrial (mtDNA) deletions have been associated with skeletal muscle atrophy and myofiber loss. However, whether such defects occurring in myofibers cause sarcopenia is unclear. Also, the contribution of mtDNA alterations in muscle stem cells (MuSCs) to sarcopenia remain to be investigated. We expressed a dominant-negative variant of the mitochondrial helicase, which induces mtDNA alterations, specifically in differentiated myofibers (K320Eskm mice) and MuSCs (K320Emsc mice), respectively, and investigated their impact on muscle structure and function by immunohistochemistry, analysis of mtDNA and respiratory chain content, muscle transcriptome and functional tests. K320Eskm mice at 24 months of age had higher levels of mtDNA deletions compared to controls in soleus (SOL, 0.07673 % vs 0.00015 %, p=0.0167), extensor digitorium longi (EDL, 0.0649 vs 0.000925, p= 0.0015) and gastrocnemius (GAS, 0.09353 vs 0.000425, p=0.0004). K320Eskm mice revealed a progressive increase in the proportion of cytochrome c oxidase deficient fibers (COX-) in cross sections, reaching a maximum of 3.03%, 4.36%, 13.58% and 17.08% in EDL, SOL, tibialis anterior (TA) and GAS, respectively. However, mice did not show accelerated loss of muscle mass, muscle strength or physical performance. Histological analyses revealed ragged red fibers but also stimulated regeneration, indicating activation of MuSCs. RNAseq demonstrated enhanced expression of genes associated with protein synthesis, but also degradation, as well as muscle fiber differentiation and cell proliferation. In contrast, 7 days after destruction by cardiotoxin, regenerating TA of K320Emsc mice showed 30% of COX- fibers. Notably, regenerated muscle showed dystrophic changes, increased fibrosis (2.5% vs 1.6%, p=0.0003), increased abundance of fat cells (2.76% vs 0.23%, p=0.0144) and reduced muscle mass (regenerated TA: 40.0mg vs 60.2mg, p=0.0171). In contrast to muscles from K320Eskm mice, freshly isolated MuSCs from aged K320Emsc mice were completely devoid of mtDNA alterations. However, after passaging, mtDNA copy number as well as respiratory chain subunits and p62 levels gradually decreased.Taken together, accumulation of large-scale mtDNA alterations in myofibers alone is not sufficient to cause sarcopenia. Expression of K320E is tolerated in quiescent MuSCs, but progressively leads to mtDNA and respiratory chain depletion upon activation, in vivo and in vitro, possibly caused by an increased mitochondrial removal. Altogether, our results suggest that the accumulation of mtDNA alterations in myofibers activates regeneration during aging, which leads to sarcopenia if such alterations have expanded in MuSCs as well.
2022-03-26 | GSE199201 | GEO
Project description:Interventions: Colorectal cancer with sarcopenia group:None;Colorectal cancer without sarcopenia group:None;Colorectal cancer combined with malnutrition group:None;Colorectal cancer without malnutrition group:None
Primary outcome(s): Body mass index;Prognostic nutritional index;Neutrophil/lymphocyte ratio;Systemic immune inflammation index;Skeletal muscle mass index;Calf circumference;Tumor markers
Study Design: Factorial
| 2762000 | ecrin-mdr-crc
Project description:We examined age-dependent expression of the heart and neural crest derivative 2(Hand2), a critical transcription factor for post mitotic maintenance of SNs, and tested the possibility that inducing its expression exclusively in SNs will significantly prevent (a) motor denervation, (b) impaired NMJ transmission, and (d) loss of muscle mass and function in old mice
2020-06-03 | GSE151628 | GEO