对Fujie等人的“阻力训练和鸡肉摄入对老年妇女血管和肌肉健康的影响”的评论。

IF 9.4 1区 医学 Q1 GERIATRICS & GERONTOLOGY
Jiawei Du, Jinghua Hou
{"title":"对Fujie等人的“阻力训练和鸡肉摄入对老年妇女血管和肌肉健康的影响”的评论。","authors":"Jiawei Du,&nbsp;Jinghua Hou","doi":"10.1002/jcsm.13768","DOIUrl":null,"url":null,"abstract":"<p>We carefully read the article by Fujie et al., titled ‘Impact of resistance training and chicken intake on vascular and muscle health in elderly women’ [<span>1</span>], published in the <i>Journal of Cachexia, Sarcopenia and Muscle</i>. The study investigated the effects of moderate-to-high-intensity resistance training combined with a high-protein diet (steamed chicken breast) on muscle mass, strength and arterial stiffness in elderly women. The findings suggest that high-protein intake significantly mitigates the resistance training-induced increase in arterial stiffness while further enhancing muscle health indicators, offering critical insights into clinical and public health implications. However, upon in-depth analysis, we believe that several key limitations in the study design, methodology, mechanistic exploration and statistical analysis may affect the reliability of the conclusions and their clinical translational value.</p><p>First, the study employed carotid-femoral pulse wave velocity (cfPWV) and carotid β-stiffness as the primary indicators of arterial stiffness, whereas muscle mass was assessed via ultrasound measurements of muscle thickness and echo intensity (EI). However, the descriptions of these measurement methods are entirely absent. For instance, the specific equipment used for cfPWV, the exact locations for signal acquisition and the standardized procedures for calculating time differences were not provided. Similarly, the ultrasound measurements of muscle thickness and EI lacked details on probe frequency, participant positioning and standardized protocols for repeated measurements. This lack of methodological detail may hinder the reproducibility of the study by other researchers and undermine the credibility and generalizability of the findings. We recommend supplementing the study with detailed descriptions of experimental procedures and referencing internationally recognized standards (e.g., guidelines from the European Society of Hypertension or the American Institute of Ultrasound in Medicine) to ensure transparency and reproducibility.</p><p>Second, the study did not assess the potential impact of high-protein intake on renal function (e.g., glomerular filtration rate [GFR]) or discuss the potential risks of long-term high-protein consumption, such as hyperuricemia or metabolic acidosis. Whereas high-protein diets have significant benefits for muscle health, long-term high-protein intake may impose additional renal burden, particularly in elderly populations with potentially declining renal function [<span>2</span>]. The nitrogenous waste produced by protein metabolism requires renal excretion, and prolonged high-protein intake may accelerate renal function decline. Studies have shown that high-protein diets may increase the risk of renal function deterioration in patients with chronic kidney disease (CKD) [<span>3</span>]. Additionally, high-protein diets may lead to metabolic acidosis, especially in the elderly, as the acidic byproducts of protein metabolism may exceed the body's buffering capacity, resulting in decreased blood pH [<span>4</span>]. Future studies should evaluate the effects of high-protein intake on renal and metabolic health and explore individualized nutritional strategies to maximize benefits while minimizing risks.</p><p>Third, the study only mentioned angiotensin II (Ang II) as a potential mechanism for the resistance training-induced increase in arterial stiffness but did not explore other underlying mechanisms, such as oxidative stress and inflammation. Previous research has shown that oxidative stress and inflammation are significant drivers of arterial stiffness [<span>5</span>]. Resistance training may increase reactive oxygen species (ROS) production, leading to oxidative stress and endothelial cell damage, thereby exacerbating arterial stiffness [<span>6</span>]. Ang II, through the activation of NADPH oxidase, increases ROS production, contributing to oxidative stress and vascular damage [<span>5</span>]. However, the study did not measure markers of oxidative stress and inflammation (e.g., MDA, SOD, CRP and IL-6), which could provide valuable insights into the pathways by which resistance training impacts vascular health. These markers could have been measured using the existing serum samples. Furthermore, elevated Ang II levels may impair endothelium-dependent vasodilation by reducing nitric oxide (NO) bioavailability, further exacerbating vascular stiffness. By incorporating measurements of oxidative stress and inflammatory markers and exploring the interactions between Ang II and other mechanisms, the study could provide a more comprehensive understanding of the effects of resistance training and high-protein intake on vascular health.</p><p>In terms of statistical analysis, the study performed multiple group comparisons but did not clearly state whether comprehensive corrections for multiple comparisons were applied. Additionally, the study reported only <i>p</i> values without effect sizes (e.g., Cohen's <i>d</i> or η<sup>2</sup>) or 95% confidence intervals, which may lead to an overreliance on statistical significance while neglecting the clinical significance of the intervention effects. Reporting effect sizes would help clarify the magnitude of the intervention effects and better assess their translational value. Although the Bonferroni correction is conservative, it may increase the risk of Type II errors (false negatives). More flexible multiple comparison correction methods, such as Tukey HSD or Holm correction, may be more suitable for this type of study. We recommend enhancing the rigour of statistical analysis and the interpretability of the results.</p><p>Despite these limitations, Fujie et al.'s study is innovative in exploring the synergistic effects of resistance training and high-protein diets on muscle and vascular health in elderly populations. The findings provide preliminary evidence for comprehensive intervention strategy to improve muscle health and mitigate adverse vascular effects induced by resistance training. We look forward to the authors' responses to these concerns and hope that future research will comprehensively explore the long-term effects of resistance training and high-protein diets in elderly populations, thereby enhancing the scientific validity and translational value of such studies.</p><p>Conceptualization: Jiawei Du and Jinghua Hou. Writing – original draft: Jiawei Du. Writing – review and editing: Jinghua Hou. All authors have read and consented to the publication of this manuscript.</p><p>The authors declare no conflicts of interest.</p>","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 2","pages":""},"PeriodicalIF":9.4000,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13768","citationCount":"0","resultStr":"{\"title\":\"Comment on ‘Impact of Resistance Training and Chicken Intake on Vascular and Muscle Health in Elderly Women’ by Fujie et al.\",\"authors\":\"Jiawei Du,&nbsp;Jinghua Hou\",\"doi\":\"10.1002/jcsm.13768\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>We carefully read the article by Fujie et al., titled ‘Impact of resistance training and chicken intake on vascular and muscle health in elderly women’ [<span>1</span>], published in the <i>Journal of Cachexia, Sarcopenia and Muscle</i>. The study investigated the effects of moderate-to-high-intensity resistance training combined with a high-protein diet (steamed chicken breast) on muscle mass, strength and arterial stiffness in elderly women. The findings suggest that high-protein intake significantly mitigates the resistance training-induced increase in arterial stiffness while further enhancing muscle health indicators, offering critical insights into clinical and public health implications. However, upon in-depth analysis, we believe that several key limitations in the study design, methodology, mechanistic exploration and statistical analysis may affect the reliability of the conclusions and their clinical translational value.</p><p>First, the study employed carotid-femoral pulse wave velocity (cfPWV) and carotid β-stiffness as the primary indicators of arterial stiffness, whereas muscle mass was assessed via ultrasound measurements of muscle thickness and echo intensity (EI). However, the descriptions of these measurement methods are entirely absent. For instance, the specific equipment used for cfPWV, the exact locations for signal acquisition and the standardized procedures for calculating time differences were not provided. Similarly, the ultrasound measurements of muscle thickness and EI lacked details on probe frequency, participant positioning and standardized protocols for repeated measurements. This lack of methodological detail may hinder the reproducibility of the study by other researchers and undermine the credibility and generalizability of the findings. We recommend supplementing the study with detailed descriptions of experimental procedures and referencing internationally recognized standards (e.g., guidelines from the European Society of Hypertension or the American Institute of Ultrasound in Medicine) to ensure transparency and reproducibility.</p><p>Second, the study did not assess the potential impact of high-protein intake on renal function (e.g., glomerular filtration rate [GFR]) or discuss the potential risks of long-term high-protein consumption, such as hyperuricemia or metabolic acidosis. Whereas high-protein diets have significant benefits for muscle health, long-term high-protein intake may impose additional renal burden, particularly in elderly populations with potentially declining renal function [<span>2</span>]. The nitrogenous waste produced by protein metabolism requires renal excretion, and prolonged high-protein intake may accelerate renal function decline. Studies have shown that high-protein diets may increase the risk of renal function deterioration in patients with chronic kidney disease (CKD) [<span>3</span>]. Additionally, high-protein diets may lead to metabolic acidosis, especially in the elderly, as the acidic byproducts of protein metabolism may exceed the body's buffering capacity, resulting in decreased blood pH [<span>4</span>]. Future studies should evaluate the effects of high-protein intake on renal and metabolic health and explore individualized nutritional strategies to maximize benefits while minimizing risks.</p><p>Third, the study only mentioned angiotensin II (Ang II) as a potential mechanism for the resistance training-induced increase in arterial stiffness but did not explore other underlying mechanisms, such as oxidative stress and inflammation. Previous research has shown that oxidative stress and inflammation are significant drivers of arterial stiffness [<span>5</span>]. Resistance training may increase reactive oxygen species (ROS) production, leading to oxidative stress and endothelial cell damage, thereby exacerbating arterial stiffness [<span>6</span>]. Ang II, through the activation of NADPH oxidase, increases ROS production, contributing to oxidative stress and vascular damage [<span>5</span>]. However, the study did not measure markers of oxidative stress and inflammation (e.g., MDA, SOD, CRP and IL-6), which could provide valuable insights into the pathways by which resistance training impacts vascular health. These markers could have been measured using the existing serum samples. Furthermore, elevated Ang II levels may impair endothelium-dependent vasodilation by reducing nitric oxide (NO) bioavailability, further exacerbating vascular stiffness. By incorporating measurements of oxidative stress and inflammatory markers and exploring the interactions between Ang II and other mechanisms, the study could provide a more comprehensive understanding of the effects of resistance training and high-protein intake on vascular health.</p><p>In terms of statistical analysis, the study performed multiple group comparisons but did not clearly state whether comprehensive corrections for multiple comparisons were applied. Additionally, the study reported only <i>p</i> values without effect sizes (e.g., Cohen's <i>d</i> or η<sup>2</sup>) or 95% confidence intervals, which may lead to an overreliance on statistical significance while neglecting the clinical significance of the intervention effects. Reporting effect sizes would help clarify the magnitude of the intervention effects and better assess their translational value. Although the Bonferroni correction is conservative, it may increase the risk of Type II errors (false negatives). More flexible multiple comparison correction methods, such as Tukey HSD or Holm correction, may be more suitable for this type of study. We recommend enhancing the rigour of statistical analysis and the interpretability of the results.</p><p>Despite these limitations, Fujie et al.'s study is innovative in exploring the synergistic effects of resistance training and high-protein diets on muscle and vascular health in elderly populations. The findings provide preliminary evidence for comprehensive intervention strategy to improve muscle health and mitigate adverse vascular effects induced by resistance training. We look forward to the authors' responses to these concerns and hope that future research will comprehensively explore the long-term effects of resistance training and high-protein diets in elderly populations, thereby enhancing the scientific validity and translational value of such studies.</p><p>Conceptualization: Jiawei Du and Jinghua Hou. Writing – original draft: Jiawei Du. Writing – review and editing: Jinghua Hou. All authors have read and consented to the publication of this manuscript.</p><p>The authors declare no conflicts of interest.</p>\",\"PeriodicalId\":48911,\"journal\":{\"name\":\"Journal of Cachexia Sarcopenia and Muscle\",\"volume\":\"16 2\",\"pages\":\"\"},\"PeriodicalIF\":9.4000,\"publicationDate\":\"2025-03-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13768\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Cachexia Sarcopenia and Muscle\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/jcsm.13768\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"GERIATRICS & GERONTOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cachexia Sarcopenia and Muscle","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jcsm.13768","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

我们仔细阅读了Fujie等人发表在《恶病质、肌肉减少症和肌肉杂志》上的文章,题为“阻力训练和鸡肉摄入对老年妇女血管和肌肉健康的影响”。该研究调查了中高强度抗阻训练与高蛋白饮食(蒸鸡胸肉)对老年妇女肌肉质量、力量和动脉僵硬的影响。研究结果表明,高蛋白摄入显著减轻了阻力训练引起的动脉僵硬增加,同时进一步增强了肌肉健康指标,为临床和公共卫生影响提供了重要见解。然而,经过深入分析,我们认为在研究设计、方法学、机制探索和统计分析方面的几个关键限制可能会影响结论的可靠性及其临床转化价值。首先,该研究采用颈动脉-股动脉脉搏波速度(cfPWV)和颈动脉β-刚度作为动脉刚度的主要指标,而肌肉质量则通过超声测量肌肉厚度和回声强度(EI)来评估。然而,这些测量方法的描述是完全缺失的。例如,cfPWV使用的具体设备、信号采集的确切位置和计算时差的标准化程序都没有提供。同样,肌肉厚度和EI的超声测量缺乏探针频率、参与者定位和重复测量的标准化方案的细节。方法细节的缺乏可能会阻碍其他研究人员对研究的可重复性,并破坏研究结果的可信度和普遍性。我们建议对研究进行补充,详细描述实验过程,并参考国际公认的标准(例如,欧洲高血压学会或美国超声医学研究所的指南),以确保透明度和可重复性。其次,该研究没有评估高蛋白摄入对肾功能的潜在影响(如肾小球滤过率[GFR]),也没有讨论长期高蛋白摄入的潜在风险,如高尿酸血症或代谢性酸中毒。虽然高蛋白饮食对肌肉健康有显著的好处,但长期摄入高蛋白可能会增加肾脏负担,特别是在肾功能可能下降的老年人群中。蛋白质代谢产生的含氮废物需要肾脏排泄,长期摄入高蛋白会加速肾功能下降。研究表明,高蛋白饮食可能会增加慢性肾病(CKD)患者肾功能恶化的风险。此外,高蛋白饮食可能导致代谢性酸中毒,特别是在老年人中,因为蛋白质代谢的酸性副产物可能超过身体的缓冲能力,导致血液pH值下降。未来的研究应评估高蛋白摄入对肾脏和代谢健康的影响,并探索个性化的营养策略,以最大限度地提高益处,同时降低风险。第三,该研究仅提到血管紧张素II (Ang II)作为阻力训练诱导的动脉僵硬增加的潜在机制,而没有探索其他潜在机制,如氧化应激和炎症。先前的研究表明,氧化应激和炎症是动脉硬化的重要驱动因素。抗阻训练可能增加活性氧(ROS)的产生,导致氧化应激和内皮细胞损伤,从而加剧动脉僵硬。Ang II通过激活NADPH氧化酶,增加ROS的产生,导致氧化应激和血管损伤[5]。然而,该研究没有测量氧化应激和炎症的标志物(如MDA、SOD、CRP和IL-6),这可以为阻力训练影响血管健康的途径提供有价值的见解。这些标记物可以用现有的血清样本来测量。此外,升高的Ang II水平可能通过降低一氧化氮(NO)的生物利用度而损害内皮依赖性血管舒张,进一步加剧血管僵硬。通过结合氧化应激和炎症标志物的测量,以及探索Ang II与其他机制之间的相互作用,该研究可以更全面地了解阻力训练和高蛋白摄入对血管健康的影响。在统计分析方面,本研究进行了多组比较,但没有明确说明是否对多组比较进行了综合校正。此外,该研究仅报告了p值,没有效应量(例如: 如Cohen’s d or η2)或95%置信区间,可能导致过度依赖统计显著性而忽视干预效果的临床意义。报告效果大小将有助于澄清干预效果的大小,并更好地评估其转化价值。虽然Bonferroni校正是保守的,但它可能会增加II型错误(假阴性)的风险。更灵活的多重比较校正方法,如Tukey HSD或Holm校正,可能更适合这类研究。我们建议加强统计分析的严谨性和结果的可解释性。尽管存在这些局限性,但Fujie等人的研究在探索抗阻训练和高蛋白饮食对老年人肌肉和血管健康的协同作用方面具有创新性。研究结果为综合干预策略改善肌肉健康和减轻阻力训练引起的血管不良反应提供了初步证据。我们期待着作者对这些问题的回应,希望未来的研究能够全面探索抗阻训练和高蛋白饮食对老年人的长期影响,从而提高这类研究的科学有效性和转化价值。概念:杜嘉伟、侯景华。写作-原稿:杜佳伟。写作-审编:侯景华。所有作者都已阅读并同意发表这篇稿件。作者声明无利益冲突。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Comment on ‘Impact of Resistance Training and Chicken Intake on Vascular and Muscle Health in Elderly Women’ by Fujie et al.

We carefully read the article by Fujie et al., titled ‘Impact of resistance training and chicken intake on vascular and muscle health in elderly women’ [1], published in the Journal of Cachexia, Sarcopenia and Muscle. The study investigated the effects of moderate-to-high-intensity resistance training combined with a high-protein diet (steamed chicken breast) on muscle mass, strength and arterial stiffness in elderly women. The findings suggest that high-protein intake significantly mitigates the resistance training-induced increase in arterial stiffness while further enhancing muscle health indicators, offering critical insights into clinical and public health implications. However, upon in-depth analysis, we believe that several key limitations in the study design, methodology, mechanistic exploration and statistical analysis may affect the reliability of the conclusions and their clinical translational value.

First, the study employed carotid-femoral pulse wave velocity (cfPWV) and carotid β-stiffness as the primary indicators of arterial stiffness, whereas muscle mass was assessed via ultrasound measurements of muscle thickness and echo intensity (EI). However, the descriptions of these measurement methods are entirely absent. For instance, the specific equipment used for cfPWV, the exact locations for signal acquisition and the standardized procedures for calculating time differences were not provided. Similarly, the ultrasound measurements of muscle thickness and EI lacked details on probe frequency, participant positioning and standardized protocols for repeated measurements. This lack of methodological detail may hinder the reproducibility of the study by other researchers and undermine the credibility and generalizability of the findings. We recommend supplementing the study with detailed descriptions of experimental procedures and referencing internationally recognized standards (e.g., guidelines from the European Society of Hypertension or the American Institute of Ultrasound in Medicine) to ensure transparency and reproducibility.

Second, the study did not assess the potential impact of high-protein intake on renal function (e.g., glomerular filtration rate [GFR]) or discuss the potential risks of long-term high-protein consumption, such as hyperuricemia or metabolic acidosis. Whereas high-protein diets have significant benefits for muscle health, long-term high-protein intake may impose additional renal burden, particularly in elderly populations with potentially declining renal function [2]. The nitrogenous waste produced by protein metabolism requires renal excretion, and prolonged high-protein intake may accelerate renal function decline. Studies have shown that high-protein diets may increase the risk of renal function deterioration in patients with chronic kidney disease (CKD) [3]. Additionally, high-protein diets may lead to metabolic acidosis, especially in the elderly, as the acidic byproducts of protein metabolism may exceed the body's buffering capacity, resulting in decreased blood pH [4]. Future studies should evaluate the effects of high-protein intake on renal and metabolic health and explore individualized nutritional strategies to maximize benefits while minimizing risks.

Third, the study only mentioned angiotensin II (Ang II) as a potential mechanism for the resistance training-induced increase in arterial stiffness but did not explore other underlying mechanisms, such as oxidative stress and inflammation. Previous research has shown that oxidative stress and inflammation are significant drivers of arterial stiffness [5]. Resistance training may increase reactive oxygen species (ROS) production, leading to oxidative stress and endothelial cell damage, thereby exacerbating arterial stiffness [6]. Ang II, through the activation of NADPH oxidase, increases ROS production, contributing to oxidative stress and vascular damage [5]. However, the study did not measure markers of oxidative stress and inflammation (e.g., MDA, SOD, CRP and IL-6), which could provide valuable insights into the pathways by which resistance training impacts vascular health. These markers could have been measured using the existing serum samples. Furthermore, elevated Ang II levels may impair endothelium-dependent vasodilation by reducing nitric oxide (NO) bioavailability, further exacerbating vascular stiffness. By incorporating measurements of oxidative stress and inflammatory markers and exploring the interactions between Ang II and other mechanisms, the study could provide a more comprehensive understanding of the effects of resistance training and high-protein intake on vascular health.

In terms of statistical analysis, the study performed multiple group comparisons but did not clearly state whether comprehensive corrections for multiple comparisons were applied. Additionally, the study reported only p values without effect sizes (e.g., Cohen's d or η2) or 95% confidence intervals, which may lead to an overreliance on statistical significance while neglecting the clinical significance of the intervention effects. Reporting effect sizes would help clarify the magnitude of the intervention effects and better assess their translational value. Although the Bonferroni correction is conservative, it may increase the risk of Type II errors (false negatives). More flexible multiple comparison correction methods, such as Tukey HSD or Holm correction, may be more suitable for this type of study. We recommend enhancing the rigour of statistical analysis and the interpretability of the results.

Despite these limitations, Fujie et al.'s study is innovative in exploring the synergistic effects of resistance training and high-protein diets on muscle and vascular health in elderly populations. The findings provide preliminary evidence for comprehensive intervention strategy to improve muscle health and mitigate adverse vascular effects induced by resistance training. We look forward to the authors' responses to these concerns and hope that future research will comprehensively explore the long-term effects of resistance training and high-protein diets in elderly populations, thereby enhancing the scientific validity and translational value of such studies.

Conceptualization: Jiawei Du and Jinghua Hou. Writing – original draft: Jiawei Du. Writing – review and editing: Jinghua Hou. All authors have read and consented to the publication of this manuscript.

The authors declare no conflicts of interest.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Journal of Cachexia Sarcopenia and Muscle
Journal of Cachexia Sarcopenia and Muscle MEDICINE, GENERAL & INTERNAL-
CiteScore
13.30
自引率
12.40%
发文量
234
审稿时长
16 weeks
期刊介绍: The Journal of Cachexia, Sarcopenia and Muscle is a peer-reviewed international journal dedicated to publishing materials related to cachexia and sarcopenia, as well as body composition and its physiological and pathophysiological changes across the lifespan and in response to various illnesses from all fields of life sciences. The journal aims to provide a reliable resource for professionals interested in related research or involved in the clinical care of affected patients, such as those suffering from AIDS, cancer, chronic heart failure, chronic lung disease, liver cirrhosis, chronic kidney failure, rheumatoid arthritis, or sepsis.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信