JCSM rapid communications最新文献_第6页

Publication trends and hot spots in the Journal of Cachexia, Sarcopenia and Muscle: A bibliometric analysis (2010–2022) 痛症、肌肉疏松症与肌肉杂志》的出版趋势与热点：文献计量分析（2010-2022 年）

JCSM rapid communications

Pub Date : 2024-02-29 DOI: 10.1002/rco2.88

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

Background

The Journal of Cachexia, Sarcopenia and Muscle 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.

Methods

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.

Results

From 2010 to 2022, 1194 studies were published in the Journal of Cachexia, Sarcopenia and Muscle. 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 Journal of Cachexia, Sarcopenia and Muscle was cited the most by Nutrients, and PLOS ONE was cited the most by the Journal of Cachexia, Sarcopenia and Muscle.

Conclusions

Publications in the Journal of Cachexia, Sarcopenia and Muscle 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.

背景《恶病质、肌肉疏松症与肌肉杂志》是由 WILEY 于 2010 年出版的同行评审医学季刊，一直致力于推动慢性疾病，尤其是恶病质和肌肉疏松症的研究。在过去的 12 年中，全球范围内的肌肉疏松症研究发生了重大变化。本研究旨在调查在该期刊上发表的研究的各个方面。方法我们以 "Journal of Cachexia, Sarcopenia and Muscle "为关键词，从 Web of Science 和 PubMed 数据库中检索了相关出版物。我们从研究数量、总引用次数、每项被引次数、H 指数、研究领域、文章类型、机构、国家和资助机构等不同角度对发表在该期刊上的研究进行了分类和分析。使用 VOS 浏览器软件进行共现、书目耦合、共引和合著分析。结果从 2010 年到 2022 年，《痛症、肉质疏松症和肌肉杂志》共发表了 1194 篇研究论文。美国是贡献最多的国家，发表的论文最多，被引用的次数最多，H 指数也最高。意大利的单篇引用次数排名第一。von Haehling S 是影响最大的作者。美国国立卫生研究院和美国卫生人类服务部资助的研究数量最多。12 年来，所有出版物中使用频率最高的 5 个关键词是肌肉疏松症、恶病质、骨骼肌、身体成分和肌肉质量。营养素》对《恶病质、肌肉减少症与肌肉杂志》的引用率最高，而《PLOS ONE》对《恶病质、肌肉减少症与肌肉杂志》的引用率最高。结论从2010年到2022年，《痛症、肌肉疏松症与肌肉杂志》上的论文数量显著增加，尤其是近年来。美国在肌肉疏松症研究方面仍处于领先地位。本期刊今后的投稿将继续关注肌肉疏松症、恶病质、骨骼肌、身体结构和肌肉质量。肌肉疏松症和恶病质的病因、分子机制和结果是当前的研究热点。

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引用次数: 0

Hypoxia-inducible factor prolyl hydroxylase domain inhibitors may mitigate loss of skeletal muscle mass in haemodialysis patients 缺氧诱导因子脯氨酰羟化酶结构域抑制剂可减轻血液透析患者骨骼肌质量的损失

JCSM rapid communications

Pub Date : 2024-01-04 DOI: 10.1002/rco2.87

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

Background

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.

Methods

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 Kt/V. 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.

Results

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].

Conclusions

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.

慢性肾病患者，尤其是对促红细胞生成药（ESAs）反应迟钝的肾性贫血患者，骨骼肌质量（SMM）下降的风险更大。缺氧诱导因子脯氨酰羟化酶结构域抑制剂（HIF-PHI）是一种治疗肾性贫血的新型药物，可促进血管生成、肌肉修复和平衡。然而，HIF-PHIs 对 SMM 的影响仍然未知。这项回顾性观察队列研究纳入了 292 名在我们的透析中心接受维持性血液透析的日本成年人。数据集包括在 2020 年 12 月 1 日至 2022 年 6 月 30 日期间接受达泊司他（daprodustat）治疗 6 个月或更长时间的 11 名患者。从之前发表的汇集队列中，我们在肾性贫血 HIF-PHIs 批准之前的 2018 年 8 月 1 日至 2019 年 7 月 31 日期间招募了 281 名参与者。SMM采用按年龄、性别、血清肌酐和单池Kt/V计算的改良肌酐指数（毫克/千克/天）进行评估。在 6 至 12 个月的随访期间，采用最小二乘法回归模型和混合效应模型分析了 SMM 的年度变化[ΔSMM (%)]。在最小二乘法回归模型中，HIF-PHI组的中位ΔSMM水平（IQR）为4.0%（-1.7%至9.3%），无ESA组为0.20%（-2.1%至2.1%），每周使用相当于20微克或更多达贝泊汀的高ESA组为-0.94%（-3.0%至1.3%）。在混合效应模型中，这一比例分别为-1.7%（-1.2%至3.8%）、0.09%（-1.4%至1.3%）和-0.74%（-2.0%至0.8%）。多变量线性回归模型显示，与高ESA组相比，使用HIF-PHI与更大的ΔSMM相关[最小二乘回归模型中的系数为3.737；95%置信区间（CI）为1.216-6.258，混合效应模型中的系数为1.635；95%置信区间（CI）为0.068-3.201]。HIF-PHI可最大限度地减少终末期肾病和肾性贫血患者的SMM损失。

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引用次数: 0

The role of microRNAs in critical illness—do miRs truly ‘miRror’ muscle wasting? microRNA 在危重病中的作用--miRs 真的能 "miRror "肌肉萎缩吗？

JCSM rapid communications

Pub Date : 2023-12-26 DOI: 10.1002/rco2.86

Ryosuke Sato, Stephan von Haehling

引用次数: 0

Molecular changes in skeletal muscle in chronic kidney disease: A systematic review 慢性肾脏病骨骼肌的分子变化：系统综述

JCSM rapid communications

Pub Date : 2023-12-26 DOI: 10.1002/rco2.82

Limy Wong, Rachel Kenny, Jennifer Howard, Lawrence P. McMahon

Background

Loss of skeletal muscle mass is prevalent among patients affected by chronic kidney disease (CKD). It is associated with significant morbidity and mortality. The underlying molecular pathogenesis has yet to be fully understood. The aim of this systematic review is to summarize the current evidence on molecular changes in the skeletal muscle of humans and rodents with CKD and to assess the strength of such evidence.

Methods

The PubMed and EMBASE databases were searched using three main themes: messenger ribonucleic acid/protein/microRNA expression, skeletal muscle and CKD. This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards.

Results

A total of 98 studies were included in the systematic review, comprising 26 prospective human clinical studies, four human and rodent studies, and 68 rodent-only studies (32 mouse and 36 rat models respectively). The sample sizes of human studies were largely small (40% of studies had ≤20 participants). Qualitative polymerase chain reaction (qPCR) was the most commonly used method for gene expression and none of the studies fulfilled the Minimum Information for Publication of qPCR Experiments criteria for quality assessment. Majority of the studies investigated only a few genes or a specific signalling pathway. FBXO32, TRIM63, MSTN, IL6, TNF and IGF1 were the most investigated genes. The identified differentially expressed genes and proteins belonged to eight major pathways, including apoptosis, autophagy, inflammation, insulin/insulin-like growth factor 1 signalling, lipid metabolism, mitochondrial function, muscle cell growth and differentiation, and protein degradation, similar to other chronic disease states.

Conclusions

The current evidence regarding molecular alterations in the skeletal muscle in CKD is largely derived from small and heterogenous studies. Markedly similar modifications in the major biological pathways between CKD and other chronic diseases supports shared deleterious molecular mechanisms producing muscle atrophy, irrespective of the underlying specific disease.

背景慢性肾脏病（CKD）患者普遍存在骨骼肌质量下降的问题。它与严重的发病率和死亡率有关。其潜在的分子发病机制尚未完全明了。本系统综述旨在总结目前有关 CKD 患者和啮齿类动物骨骼肌分子变化的证据，并评估这些证据的强度。方法使用三个主题对 PubMed 和 EMBASE 数据库进行检索：信使核糖核酸/蛋白质/microRNA 表达、骨骼肌和 CKD。本研究按照系统综述和荟萃分析首选报告项目（PRISMA）标准进行。结果总共有 98 项研究被纳入系统综述，其中包括 26 项前瞻性人类临床研究、4 项人类和啮齿动物研究以及 68 项纯啮齿动物研究（分别为 32 个小鼠模型和 36 个大鼠模型）。人类研究的样本量大多较小（40% 的研究参与者少于 20 人）。定性聚合酶链反应（qPCR）是最常用的基因表达方法，但没有一项研究符合《qPCR 实验发表最低信息量》的质量评估标准。大多数研究只调查了几个基因或特定的信号通路。FBXO32、TRIM63、MSTN、IL6、TNF 和 IGF1 是调查最多的基因。已确定的差异表达基因和蛋白质属于八种主要通路，包括细胞凋亡、自噬、炎症、胰岛素/胰岛素样生长因子 1 信号传导、脂质代谢、线粒体功能、肌肉细胞生长和分化以及蛋白质降解，这与其他慢性疾病状态类似。结论目前有关慢性肾脏病患者骨骼肌分子改变的证据主要来自小型和异质性研究。CKD 和其他慢性疾病的主要生物通路发生了明显的相似变化，这支持了产生肌肉萎缩的共同有害分子机制，而与潜在的特定疾病无关。

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引用次数: 0

Pharmacological inhibition of IRAK4 kinase activity does not prevent cachexia in mice with pancreatic cancer 药物抑制 IRAK4 激酶的活性并不能防止胰腺癌小鼠出现恶病质

JCSM rapid communications

Pub Date : 2023-12-26 DOI: 10.1002/rco2.85

Shuxi Qiao, Brianna LaViolette, Brianna LaCarubba Paulhus, Xiangping Li, John Litchfield, Zhenhong Li, John C. Stansfield, Richard L. Gieseck III, Bei B. Zhang, Danna M. Breen

Background

Inflammation is a hallmark of cachexia; however, effective anti-inflammatory treatments have not yet been identified. Interleukin-1 receptor-associated kinase 4 (IRAK4) is a key signalling node linking interleukin-1 receptor (IL-1R) and toll-like receptor (TLR) activation to the production of multiple proinflammatory cytokines that are elevated in cancer cachexia. The purpose of this work is to evaluate whether pharmacological inhibition of IRAK4 kinase activity with PF-06426779 could prevent cachexia using a model of pancreatic cancer. The effect of appetite stimulation via the ghrelin receptor agonist anamorelin was also examined as a benchmark of clinically validated mechanisms.

Methods

Female C57Bl/6J mice were given an intraperitoneal injection of Kras^G12D; p53^R172H; Pdx1-Cre (KPC) pancreatic tumour cells. PF-06426779 or anamorelin treatment was initiated at the onset of anorexia. Body weight and food intake were measured throughout the study. Body composition, muscle function (force), and physical activity (treadmill running endurance) were assessed at the end of the study.

Results

Chronic treatment with PF-06426779, at doses covering in vitro IC50 and IC90 at C_min, did not increase body weight, food intake, and muscle function in the KPC tumour model. In contrast, anamorelin (vs. vehicle) increased food intake (P < 0.01), hindlimb skeletal muscle mass (P < 0.01), and muscle strength (P < 0.05); however, treadmill running endurance was not increased.

Conclusions

These data suggest that inhibition of IRAK4 kinase activity is not sufficient to treat cachexia, at least in pancreatic cancer, and exploration of alternative anti-inflammatory strategies that increase appetite is required.

背景炎症是恶病质的一个特征；然而，有效的抗炎治疗方法尚未确定。白细胞介素-1受体相关激酶4（IRAK4）是连接白细胞介素-1受体（IL-1R）和收费样受体（TLR）活化与多种促炎细胞因子产生的关键信号节点，而癌症恶病质中这些细胞因子会升高。这项研究的目的是利用胰腺癌模型评估 PF-06426779 对 IRAK4 激酶活性的药理抑制能否预防恶病质。作为临床验证机制的基准，还研究了通过胃泌素受体激动剂阿那莫瑞林刺激食欲的效果。方法给雌性 C57Bl/6J 小鼠腹腔注射 KrasG12D; p53R172H; Pdx1-Cre (KPC) 胰腺肿瘤细胞。厌食症发生时开始使用 PF-06426779 或阿那莫林治疗。在整个研究过程中测量体重和食物摄入量。研究结束时对身体成分、肌肉功能（力量）和体力活动（跑步机跑步耐力）进行评估。结果在 KPC 肿瘤模型中，PF-06426779 的体外 IC50 和 Cmin IC90 剂量的慢性治疗不会增加体重、食物摄入量和肌肉功能。相反，阿那莫瑞林（与车辆相比）增加了食物摄入量（P < 0.01）、后肢骨骼肌质量（P < 0.01）和肌肉力量（P < 0.05）；但是，跑步机跑步耐力没有增加。结论这些数据表明，抑制 IRAK4 激酶活性不足以治疗恶病质，至少在胰腺癌患者中是如此，因此需要探索能增加食欲的其他抗炎策略。

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引用次数: 0

Programmed myofibre necrosis in critical illness acquired muscle wasting 危重病获得性肌肉萎缩中的程序性肌纤维坏死

JCSM rapid communications

Pub Date : 2023-12-03 DOI: 10.1002/rco2.83

Sunil Patel, Thomas Francis, Raghini Rajaram, Rhodri Handslip, Sharon Mumby, Danielle E. Bear, Rahul Padhke, Nicholas Hart, Hugh Montgomery, Masao Takata, Stephen D.R. Harridge, Brijesh V. Patel, Zudin Puthucheary

Background

Acute skeletal muscle wasting during critical illness is common and causes significant morbidity and functional limitation. Myofibre necrosis is a major histological finding but is often considered an unprogrammed by-product of muscle inflammation. This study sought to evaluate if a form of programmed necrosis, necroptosis, is activated in skeletal muscle during critical illness.

Methods

A cohort of 28 patients from the MUSCLE-UK study (ClinicalTrials.gov: NCT01106300) with serum and skeletal muscle biopsy samples were identified. Samples were available from ICU admission (T1) and between day 7–10 post admission (T2). Skeletal muscle was stratified by a histopathologist in the original study as necrotic (NEC, N = 14) or non-necrotic (NONEC, N = 14) using haematoxylin and eosin staining. We used phosphorylated mixed-lineage kinase domain-like (pMLKL) protein (a key terminal effector protein) and receptor-interacting protein kinase 3 (RIPK3) as markers of necroptosis activation using Western blotting and immunohistochemistry.

Results

We show that pMLKL expression is significantly higher in the NEC group [NEC: T2:T1 expression; 9.1 (IQR 3.9–22.3) vs. NONEC: T2:T1 expression; 0.9 (IQR 0.6–1.1), P = 0.003]. We then confirm this upregulation and describe co-localization with receptor interacting protein kinase 3 (RIPK3) in skeletal muscle using immunohistochemistry. We show that both RIPK3 and pMLKL are present within intact myofibres at the intermediate timepoint day 3 without cellular infiltrate. At T2, pMLKL is also present in the interstitial space where there is infiltrate of CD68 positive immune cells. The observed necroptosis may originate from both internal and infiltrating sources. These findings were absent in samples from patients who did not exhibit histopathological features of necrosis.

Conclusions

We show that necroptosis machinery, RIPK3 and pMLKL, are associated with conventional histopathological features of myonecrosis in a critically ill cohort.

急性骨骼肌萎缩在危重疾病期间是常见的，并引起显著的发病率和功能限制。肌纤维坏死是一种主要的组织学发现，但通常被认为是肌肉炎症的非程序性副产品。本研究旨在评估是否一种形式的程序性坏死，坏死性上睑下垂，骨骼肌在危重疾病期间被激活。来自MUSCLE‐UK研究(ClinicalTrials.gov: NCT01106300)的28例患者的血清和骨骼肌活检样本被确定。样本可从ICU入院(T1)和入院后7-10天(T2)获得。在最初的研究中，组织病理学家使用血红素和伊红染色将骨骼肌分层为坏死(NEC, N = 14)或非坏死(NONEC, N = 14)。我们使用磷酸化的混合谱系激酶结构域样蛋白(pMLKL)(一种关键的末端效应蛋白)和受体相互作用蛋白激酶3 (RIPK3)作为necroptosis激活的标记物，使用Western blotting和免疫组织化学。我们发现pMLKL的表达在NEC组中显著升高[NEC: T2:T1表达;9.1 (IQR 3.9-22.3) vs. NONEC: T2:T1表达;0.9 (iqr 0.6 ~ 1.1)， p = 0.003]。然后，我们用免疫组织化学方法证实了这种上调，并描述了骨骼肌中受体相互作用蛋白激酶3 (RIPK3)的共定位。我们发现RIPK3和pMLKL在没有细胞浸润的情况下，在第3天的中间时间点存在于完整的肌纤维中。T2时，pMLKL也存在于CD68阳性免疫细胞浸润的间质间隙。观察到的坏死性下垂可能来源于内部和浸润性来源。这些发现在没有表现出坏死组织病理特征的患者样本中是不存在的。我们发现坏死坏死机制RIPK3和pMLKL与危重患者群体中肌坏死的常规组织病理学特征相关。

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引用次数: 0

Relationship between sacral-abdominal wall distance and grip strength in postmenopausal osteoporotic patients 绝经后骨质疏松症患者骶腹壁距离与握力之间的关系

JCSM rapid communications

Pub Date : 2023-09-11 DOI: 10.1002/rco2.81

Takashi Nagai, Makoto Miyagami, Shota Nakamura, Yayoi Amemiya, Ichiro Okano, Keizo Sakamoto, Kasai Fumihito, Yoshifumi Kudo, Katsunori Inagaki, Nobuyuki Kawate

Background

An increase in waist circumference (WC) is a factor in lifestyle-related diseases. The rectus abdominis muscle is a skeletal muscle that attaches to the pelvis from the xiphoid process and is thought to be affected by kyphosis deformity and posterior pelvic tilt. The purpose of this study is to examine differences between sacral-abdominal wall distance (SAD) and WC and to determine whether they are associated with fall risk, frailty, markers of sarcopenia (grip strength and lean body mass), and spinal alignment. A secondary objective is to examine these differences by stratification by grip strength.

Methods

This retrospective study included 239 women aged 65 years or older (mean age 76.5 ± 6.7 years) attending an outpatient osteoporosis clinic. Bone mineral density and skeletal body composition (muscle mass index and trunk lean mass) were measured using dual-energy X-ray absorptiometry. SAD, pelvic tilt, and sagittal longitudinal axis were measured from simple X-ray images of the spine sides. WC, grip strength, frailty, and fall risk score were investigated. Statistics were performed using Stat Flex, with two-sided P < 0.05 being significantly different.

Results

WC was correlated with SAD (R = 0.68, P < 0.001). The SAD cut-off value for a WC of 90 cm was 167 mm. The relationship between grip strength, SAD, and WC, weaker grip strength was associated with greater SAD; however, no significant difference was noted in WC. WC was not correlated with pelvic alignment but was correlated with body mass index (P < 0.01). Meanwhile, SAD was correlated with body mass index, pelvic tilt, sagittal longitudinal axis (P < 0.01), spinal alignment, and WC. Logistic regression analysis was performed with a grip strength of less than 18 kg as the objective variable. We found that the conditions for a grip strength of less than 18 kg were older age (P < 0.001), increased SAD (P = 0.02), and decreased trunk lean body mass. There was a decrease in grip strength (P < 0.05) and an increase in frailty (P < 0.05) and falls (P < 0.01) score in patients with SAD of 167 mm or greater.

Conclusions

SAD and WC were found to be correlated; SAD was associated with body weight, posterior pelvic tilt, and anterior spinal tilt deformity, while WC was related to body weight. Increased SAD was found to be linked with decreased grip strength a

背景腰围（WC）的增加是导致生活方式相关疾病的一个因素。腹直肌是从剑突附着于骨盆的骨骼肌，被认为会受到脊柱后凸畸形和骨盆后倾的影响。本研究的目的是检查骶腹壁距离（SAD）和腹围之间的差异，并确定它们是否与跌倒风险、虚弱程度、肌肉疏松症指标（握力和瘦体重）以及脊柱排列有关。次要目的是通过握力分层来研究这些差异。方法这项回顾性研究包括 239 名 65 岁或以上（平均年龄 76.5 ± 6.7 岁）的女性骨质疏松症门诊患者。使用双能 X 射线吸收测量法测量了骨质密度和骨骼身体成分（肌肉质量指数和躯干瘦体重）。通过脊柱两侧的简单 X 光图像测量了 SAD、骨盆倾斜度和矢状纵轴。对体重、握力、虚弱程度和跌倒风险评分进行了调查。使用 Stat Flex 进行统计，双侧 P < 0.05 为显著差异。结果 WC 与 SAD 相关（R = 0.68，P < 0.001）。WC 为 90 厘米的 SAD 临界值为 167 毫米。从握力、SAD 和 WC 之间的关系来看，握力越弱，SAD 越大；但 WC 没有显著差异。腹围与骨盆排列无关，但与体重指数相关（P < 0.01）。同时，SAD 与体重指数、骨盆倾斜、矢状纵轴（P < 0.01）、脊柱排列和腹围相关。以握力小于 18 公斤为客观变量进行了逻辑回归分析。我们发现，握力小于 18 公斤的条件是年龄较大（P < 0.001）、SAD 增加（P = 0.02）和躯干瘦体重减少。在 SAD 达到或超过 167 毫米的患者中，握力下降（P < 0.05），虚弱（P < 0.05）和跌倒（P < 0.01）评分增加。结论 SAD 和 WC 存在相关性；SAD 与体重、骨盆后倾和脊柱前倾畸形相关，而 WC 与体重相关。研究发现，SAD 的增加与握力下降和跌倒风险增加有关。这项研究首次检验了一种新的测量方法--SAD，以评估其在握力、脊柱排列、虚弱和跌倒风险方面的实用性。

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引用次数: 0

The role of microRNAs in muscle wasting and recovery during critical illness: a systematic review microRNAs在危重疾病期间肌肉萎缩和恢复中的作用:系统综述

JCSM rapid communications

Pub Date : 2023-08-17 DOI: 10.1002/rco2.80

Maria Borja-Gonzalez, Sarah Coyne, Sarah Fagan, Jose C. Casas-Martinez, Anthony J. Sannicandro, Bairbre McNicholas, Kevin O'Connell, John G. Laffey, Rónán O'Caoimh, Brian McDonagh, Katarzyna Goljanek-Whysall

Introduction

Critical illness associated with intensive care unit (ICU) admission often results in persistent skeletal muscle wasting and may lead to frailty in older and patients with multi-morbidity. Early recognition of patients at high-risk of long-term complications could provide opportunities to minimize the impact of critical illness and improve health and quality of life. MicroRNAs (miRs) are short, non-coding RNAs that regulate approximately two-thirds of the human genome and are involved in most biological processes. Multiple studies have demonstrated their role in muscle development and disease and their potential as biomarkers of muscle wasting.

Aim and methods

This systematic review examined the potential of miRs as biomarkers and therapeutics for muscle wasting during and following critical illness. PubMed and Scopus databases were searched for terms associated with critical illness, ICU, muscle wasting, frailty and microRNAs from inception to June 2022 (PROSPERO number CRD42022339531).

Results

Out of 537 articles, seven studies met the inclusion criteria and examined skeletal muscle and circulating miRs in the context of muscle wasting and/or frailty related to critical illness. Across the seven studies, 27 different miRs were identified that were reported to be dysregulated in the muscle and four in the blood, plasma or serum of critically ill patients. Four miRs were reported to be altered in both muscle and blood during critical illness and their levels moderately correlated with parameters of muscle function. These included canonical muscle-enriched miRs (myomiRs), such as miR-133, miR-1 and miR-181, which correlated with muscle strength in critically ill patients. However, most of the miRs reported to be dysregulated in the muscle following critical illness were examined in one article only.

Conclusions

This systematic review highlights the potential of miRs as biomarkers of skeletal muscle wasting and ICU-associated weakness following critical illness, suggesting the need for larger validation studies using unbiased techniques. We have described circulating and muscle microRNAs, which correlated with muscle parameters during critical illness. However, the limited number of studies in this area highlights the requirement for further studies before these could be considered in clinical practice.

与重症监护室（ICU）入院相关的危重症通常会导致持续的骨骼肌萎缩，并可能导致老年人和多发病患者的虚弱。早期识别长期并发症高危患者可以提供机会，最大限度地减少危重症的影响，改善健康和生活质量。微小RNA（miRs）是一种短的非编码RNA，调节大约三分之二的人类基因组，并参与大多数生物过程。多项研究已经证明了它们在肌肉发育和疾病中的作用，以及它们作为肌肉萎缩生物标志物的潜力。这篇系统综述考察了miR作为生物标志物和治疗危重症期间和之后肌肉萎缩的潜力。PubMed和Scopus数据库检索了从开始到2022年6月与危重症、ICU、肌肉萎缩、虚弱和微小RNA相关的术语（PROSPERO编号CRD42022339531）。在537篇文章中，有7项研究符合纳入标准，并在与危重症相关的肌肉萎缩和/或虚弱的背景下检查了骨骼肌和循环miR。在这七项研究中，发现了27种不同的miR，据报道，它们在危重患者的肌肉中失调，在血液、血浆或血清中失调。据报道，在危重症期间，肌肉和血液中有四种miR发生了改变，它们的水平与肌肉功能参数适度相关。其中包括典型的富含肌肉的miR（myomiRs），如miR-133、miR-1和miR-181，它们与危重患者的肌肉力量相关。然而，据报道，大多数miR在危重症后肌肉中失调，仅在一篇文章中进行了检测。这篇系统综述强调了miR作为危重症后骨骼肌萎缩和ICU相关虚弱的生物标志物的潜力，表明需要使用无偏技术进行更大规模的验证研究。我们已经描述了循环和肌肉微小RNA，它们与危重症期间的肌肉参数相关。然而，该领域的研究数量有限，这突出了在临床实践中考虑这些研究之前需要进一步研究。

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引用次数: 0

Exercise intervention during chemotherapy for pancreatic cancer: Changes in body composition and function 胰腺癌化疗期间的运动干预:身体成分和功能的变化

JCSM rapid communications

Pub Date : 2023-05-03 DOI: 10.1002/rco2.74

Kathryn H. Schmitz, Robert D. Boutin, James P. Yoon, Melanie Potiaumpai, Leon Lenchik, Carissa M. White, Victor Chang

Background

Patients with pancreatic cancer often lose weight during chemotherapy with associated changes in body composition. The goal of the present analysis was to describe changes in body composition in pancreatic cancer patients on an exercise regimen. The long-term goal is to determine whether an exercise intervention may attenuate changes in body composition and function.

Methods

Twenty-two pancreatic cancer patients of all stages who were to receive chemotherapy were recruited into a pre-post exercise intervention study. A standard exercise prescription was individualized to include aerobic, resistance, stretch, and balance exercises. Pre- and post-intervention computed tomography-derived measures of body composition [skeletal muscle index (SMI), skeletal muscle density, visceral fat area, and subcutaneous fat area] and physical function measures (grip strength, timed up and go, 30-s chair stand, and tandem balance stand) were evaluated using paired t-tests, χ² tests, and Pearson correlation coefficients.

Results

The subjects were, on average, 62 years of age, 55% were female, 95% non-Hispanic White, and 45% were Stage IV. Body composition changes included a median 4.6% decrease in SMI (P = 0.04), 7.91% increase in skeletal muscle density (P = 0.05), 25.07% decrease in visceral fat area (P = 0.0001), and 22.08% decrease in subcutaneous fat area (P = 0.001). Adherence to aerobic and strength exercise was 65% and 57%, respectively. Some physical function measures improved, though not significantly: chair stands increased from a mean of 11.5 to 13.0 (P = 0.59) and timed up and go improved from a mean of 11.7 to 10.3 (P = 0.26). Change in right hand grip strength was marginally positively associated with changes in SMI (r = 0.53, P = 0.06). Improvements in skeletal muscle density were seen in 63% of patients, including Stage IV patients but did not correlate with change in function.

Conclusions

Exercise is feasible during neoadjuvant chemotherapy for pancreatic cancer patients of all stages and may assist with maintaining physical function and improving body composition. Further research is needed.

癌症胰腺癌患者通常在化疗期间体重减轻，并伴有身体成分的变化。本分析的目的是描述癌症患者在运动方案下身体成分的变化。长期目标是确定运动干预是否可以减弱身体成分和功能的变化。

{"title":"Exercise intervention during chemotherapy for pancreatic cancer: Changes in body composition and function","authors":"Kathryn H. Schmitz, Robert D. Boutin, James P. Yoon, Melanie Potiaumpai, Leon Lenchik, Carissa M. White, Victor Chang","doi":"10.1002/rco2.74","DOIUrl":"10.1002/rco2.74","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patients with pancreatic cancer often lose weight during chemotherapy with associated changes in body composition. The goal of the present analysis was to describe changes in body composition in pancreatic cancer patients on an exercise regimen. The long-term goal is to determine whether an exercise intervention may attenuate changes in body composition and function.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Twenty-two pancreatic cancer patients of all stages who were to receive chemotherapy were recruited into a pre-post exercise intervention study. A standard exercise prescription was individualized to include aerobic, resistance, stretch, and balance exercises. Pre- and post-intervention computed tomography-derived measures of body composition [skeletal muscle index (SMI), skeletal muscle density, visceral fat area, and subcutaneous fat area] and physical function measures (grip strength, timed up and go, 30-s chair stand, and tandem balance stand) were evaluated using paired <i>t</i>-tests, χ<sup>2</sup> tests, and Pearson correlation coefficients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The subjects were, on average, 62 years of age, 55% were female, 95% non-Hispanic White, and 45% were Stage IV. Body composition changes included a median 4.6% decrease in SMI (<i>P</i> = 0.04), 7.91% increase in skeletal muscle density (<i>P</i> = 0.05), 25.07% decrease in visceral fat area (<i>P</i> = 0.0001), and 22.08% decrease in subcutaneous fat area (<i>P</i> = 0.001). Adherence to aerobic and strength exercise was 65% and 57%, respectively. Some physical function measures improved, though not significantly: chair stands increased from a mean of 11.5 to 13.0 (<i>P</i> = 0.59) and timed up and go improved from a mean of 11.7 to 10.3 (<i>P</i> = 0.26). Change in right hand grip strength was marginally positively associated with changes in SMI (<i>r</i> = 0.53, <i>P</i> = 0.06). Improvements in skeletal muscle density were seen in 63% of patients, including Stage IV patients but did not correlate with change in function.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Exercise is feasible during neoadjuvant chemotherapy for pancreatic cancer patients of all stages and may assist with maintaining physical function and improving body composition. Further research is needed.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"6 1","pages":"33-41"},"PeriodicalIF":0.0,"publicationDate":"2023-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.74","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41846287","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}

引用次数: 0

A Toll-like receptor-4/NLRP3 inflammasome pathway promotes inflammation in skeletal muscle of chronic kidney disease patients Toll样受体- 4/NLRP3炎症小体通路促进慢性肾病患者骨骼肌炎症

JCSM rapid communications

Pub Date : 2023-03-28 DOI: 10.1002/rco2.75

Daniela Verzola, Pasquale Esposito, Samantha Milanesi, Michela Saio, Daniela Picciotto, Marco Frascio, Alessandro Laudon, Giacomo Garibotto, Giuliano Brunori, Francesca Viazzi

Background

An emerging hypothesis is that the activation of innate immunity in the muscle of patients with chronic kidney disease (CKD) is implicated in the development and progression of wasting and cachexia. We previously observed that Toll-like receptor-4 (TLR4) and its downward NF-κB-dependent pro-inflammatory pathways are activated in CKD muscle. It is however unknown if TLR4 can activate the TLR4/NOD, LRR, and pyrin domain-containing protein 3 (NLRP3) inflammasome pathway, which is implicated in cardiovascular disease and frailty, clinical settings that are commonly observed in CKD patients.

Methods

In a case–control cohort study, we hypothesized that a TLR4/NLRP3 inflammasome pathway is activated in skeletal muscle in uraemia. First, we studied the regulation TLR4/NLRP3/caspase-1 in skeletal muscle biopsies (20M/11F) obtained from 31 non-diabetic CKD5 patients (eGFR 8 ± 1 mL/min 1.73 m²) scheduled for peritoneal dialysis catheter insertion and 15 controls (10M/5F, eGFR 99 ± 6 mL/min 1.73 m²). Second, the effects of uraemic serum on the TLR4/NLRP3 inflammasome pathway were studied in C2C12 cells.

Results

In the muscle of CKD subjects, NLRP3 mRNA as well as its protein were overexpressed (by ~16-fold, respectively, P < 0.05 both vs. controls). Both IL-1β and IL-18 mRNA expressions were also up-regulated (~11.8–3.2-fold, respectively, P < 0.05). Also, cleaved caspase-1 was overexpressed in CKD muscle samples (P < 0.001 vs. controls). Both muscle NLRP3 mRNA (n = 22, r = −0.606, P < 0.01) and logIL-1 β protein (n = 26, r = −0.460, P < 0.02) were inversely associated with residual renal function, which suggests that the inflammasome is progressively activated in skeletal muscle of CKD patients as the residual renal function deteriorates. In addition, we observed that in C2C12 myotubes, uraemic serum up-regulates NLRP3 mRNA (~11-fold increase, P < 0.05), cleaved caspase-1 (by ~5-fold, P < 0.05), Il-1β mRNA (~3-fold increase, P < 0.05) and oxidative stress markers respect to normal serum. These effects were prevented by TAK-242, a selective TLR4 inhibitor.

Conclusions

Overall, our data demonstrate the activation of TLR4/NLRP3/caspase-1 inflammasome and its downward inflammatory cascade in the muscle of subjects with advanced-stage CKD and suggest targeting TLR4/NLRP3 inflammasome a

一种新出现的假说是，慢性肾脏病（CKD）患者肌肉中先天免疫的激活与消瘦和恶病质的发展和进展有关。我们之前观察到，Toll样受体-4（TLR4）及其向下的NF-κB依赖性促炎途径在CKD肌肉中被激活。然而，尚不清楚TLR4是否能激活TLR4/NOD、LRR和pyrin结构域含蛋白3（NLRP3）炎症小体途径，这与心血管疾病和虚弱有关，临床环境在CKD患者中常见。

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引用次数: 1

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