JCSM rapid communications最新文献

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Lenalidomide in cancer cachexia: a randomized trial of an anticancer drug applied for anti‐cachexia 来那度胺治疗癌症恶病质:一项抗恶病质抗癌药物的随机试验
JCSM rapid communications Pub Date : 2022-01-01 DOI: 10.1002/rco2.54
D. Blum, C. Hertler, R. Oberholzer, S. Wolf-Linder, M. Joerger, C. Driessen, F. Strasser
{"title":"Lenalidomide in cancer cachexia: a randomized trial of an anticancer drug applied for anti‐cachexia","authors":"D. Blum, C. Hertler, R. Oberholzer, S. Wolf-Linder, M. Joerger, C. Driessen, F. Strasser","doi":"10.1002/rco2.54","DOIUrl":"https://doi.org/10.1002/rco2.54","url":null,"abstract":"Cancer cachexia (CC) impacts quality of life, physical function, anticancer treatment response, and survival. Inflammation is a prominent pathomechanism of CC. This small‐scale study sets out to investigate the immunomodulatory drug lenalidomide in inflammatory CC in a randomized, double‐blind, placebo‐controlled trial.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"68 - 76"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45699965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Sarcopenic obesity and the risk of hospitalization or death from coronavirus disease 2019: findings from UK Biobank. 肌肉减少型肥胖与2019冠状病毒病住院或死亡的风险:来自英国生物银行的研究结果
JCSM rapid communications Pub Date : 2022-01-01 Epub Date: 2021-07-03 DOI: 10.1002/rco2.47
Thomas J Wilkinson, Thomas Yates, Luke A Baker, Francesco Zaccardi, Alice C Smith
{"title":"Sarcopenic obesity and the risk of hospitalization or death from coronavirus disease 2019: findings from UK Biobank.","authors":"Thomas J Wilkinson, Thomas Yates, Luke A Baker, Francesco Zaccardi, Alice C Smith","doi":"10.1002/rco2.47","DOIUrl":"10.1002/rco2.47","url":null,"abstract":"<p><strong>Background: </strong>Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2. The role of skeletal muscle mass in modulating immune response is well documented. Whilst obesity is well established as a key factor in COVID-19 and outcome, no study has examined the influence of both sarcopenia (low muscle mass) and obesity, termed 'sarcopenic obesity' on the risk of severe COVID-19.</p><p><strong>Methods: </strong>This study uses data from UK Biobank. Probable sarcopenia was defined as low handgrip strength. Sarcopenic obesity was mutually exclusively defined as the presence of obesity and low muscle mass [based on two established criteria: appendicular lean mass (ALM) adjusted for either (i) height or (ii) body mass index]. Severe COVID-19 was defined by a positive severe acute respiratory syndrome coronavirus 2 test result in a hospital setting and/or death with a primary cause reported as COVID-19. Fully adjusted logistic regression models were used to analyse the associations between sarcopenic status and severe COVID-19. This work was conducted under UK Biobank Application Number 52553.</p><p><strong>Results: </strong>We analysed data from 490 301 UK Biobank participants (median age 70.0 years, 46% male); 2203 (0.4%) had severe COVID-19. Individuals with probable sarcopenia were 64% more likely to have had severe COVID-19 (odds ratio 1.638; <i>P</i> < 0.001). Obesity increased the likelihood of severe COVID-19 by 76% (<i>P</i> < 0.001). Using either ALM index or ALM/body mass index to define low muscle mass, those with sarcopenic obesity were 2.6 times more likely to have severe COVID-19 (odds ratio 2.619; <i>P</i> < 0.001). Sarcopenia alone did not increase the risk of COVID-19.</p><p><strong>Conclusions: </strong>Sarcopenic obesity may increase the risk of severe COVID-19, over that of obesity alone. The mechanisms for this are complex but could be a result of a reduction in respiratory functioning, immune response, and ability to respond to metabolic stress.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"3-9"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8441916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39432676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis. 硫氧还蛋白-2的过表达通过抑制线粒体氧化应激和细胞凋亡来减轻年龄相关的肌肉损失
JCSM rapid communications Pub Date : 2022-01-01 Epub Date: 2022-01-14 DOI: 10.1002/rco2.57
Huibin Tang, Michael Kim, Myung Lee, Kellie Baumann, Francesca Olguin, Hao He, Yoyo Wang, Bowen Jiang, Shuhuan Fang, Jinguo Zhu, Kun Wang, Hui Xia, Yang Gao, Harrison B Konsker, Emmanuel A Fatodu, Marco Quarta, Justin Blonigan, Thomas A Rando, Joseph B Shrager
{"title":"Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis.","authors":"Huibin Tang, Michael Kim, Myung Lee, Kellie Baumann, Francesca Olguin, Hao He, Yoyo Wang, Bowen Jiang, Shuhuan Fang, Jinguo Zhu, Kun Wang, Hui Xia, Yang Gao, Harrison B Konsker, Emmanuel A Fatodu, Marco Quarta, Justin Blonigan, Thomas A Rando, Joseph B Shrager","doi":"10.1002/rco2.57","DOIUrl":"10.1002/rco2.57","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Skeletal muscle mass is regulated by intracellular anabolic and catabolic activities. Increased catabolic activity can shift the balance towards net protein breakdown and muscle atrophy. Mitochondrial oxidative stress activates catabolism and is linked to muscle loss. Reducing mitochondrial oxidative stress is thus a plausible approach to prevent muscle atrophy. We tested this concept in age-dependent muscle atrophy by genetically overexpressing the mitochondrial antioxidant thioredoxin-2 (TXN2).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We tested the functional role of TXN2 using ageing (&lt;i&gt;n&lt;/i&gt; = 7-10 per group) and denervation (&lt;i&gt;n&lt;/i&gt; = 3 per group) models in a transgenic mouse line that overexpresses TXN2. We investigated if overexpression of TXN2 blocks muscle loss in these models by examination of muscle weight, fibre size, and fibre number in young (~7 months) and aged (~26 months) TXN2-transgenic mice and controls. We studied the underlying mechanisms by mRNA and protein assays including transcriptomic profiling, western blot analysis, immunostaining, as well as succinate dehydrogenase, dihydroethidium, and terminal deoxynucleotidyl transferase dUTP nick end labelling staining.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Overexpression of TXN2 did not significantly alter the baseline skeletal muscle size, weight, fibre type distribution, or expression of mitochondrial respiratory chain components, but it did preserve muscle mass during ageing. The hindlimb muscle mass in aged TXN-transgenic mice was ~21-24% greater (in tibialis anterior, gastrocnemius/soleus combined, and tibialis anterior/extensor digitorum longus combined) than in age-matched controls (all &lt;i&gt;P&lt;/i&gt; &lt; 0.05). The reduction in both muscle fibre number (872 ± 206 vs, 637 ± 256 fibres in extensor digitorum longus muscle, &lt;i&gt;P&lt;/i&gt; &lt; 0.05) and muscle fibre size (1959 ± 296 vs. 1477 ± 564 μm&lt;sup&gt;2&lt;/sup&gt; in tibialis anterior muscle, &lt;i&gt;P&lt;/i&gt; &lt; 0.05) seen in young vs. aged control muscles was not significant in young vs. aged TXN-transgenic mice (both &lt;i&gt;P&lt;/i&gt; &gt; 0.05). Transcriptomic analysis revealed that catabolic genes that are up-regulated in ageing muscle, including those subserving apoptosis and the ubiquitin-like conjugation system, were normalized by TXN2 overexpression. Further, overexpressing TXN2 suppressed oxidative stress and caspase-9/3-mediated apoptotic signalling in the aged muscle at the protein level. Although denervation and its effects have been considered a component of age-related muscle atrophy, TXN2 overexpression failed to attenuate atrophy in an acute denervation model (TXN-transgenic vs. control mice, &lt;i&gt;P&lt;/i&gt; &gt; 0.05), despite preventing denervation-induced oxidative stress and apoptosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Mitochondrial oxidative stress appears to play a crucial role in effecting chronic age-dependent, but not acute neurogenic, muscle atrophy. Increased TXN2 protects muscle against oxidative stress-associated catabolic ac","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"130-145"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11995840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43062471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Muscle wasting in cancer: opportunities and challenges for exercise in clinical cancer trials. 癌症中的肌肉萎缩:癌症临床试验中锻炼的机遇和挑战。
JCSM rapid communications Pub Date : 2022-01-01 Epub Date: 2021-12-22 DOI: 10.1002/rco2.56
Ciaran M Fairman, Simon Lønbro, Thomas D Cardaci, Brandon N VanderVeen, Tormod S Nilsen, Angela E Murphy
{"title":"Muscle wasting in cancer: opportunities and challenges for exercise in clinical cancer trials.","authors":"Ciaran M Fairman,&nbsp;Simon Lønbro,&nbsp;Thomas D Cardaci,&nbsp;Brandon N VanderVeen,&nbsp;Tormod S Nilsen,&nbsp;Angela E Murphy","doi":"10.1002/rco2.56","DOIUrl":"https://doi.org/10.1002/rco2.56","url":null,"abstract":"<p><strong>Background: </strong>Low muscle in cancer is associated with an increase in treatment-related toxicities and is a predictor of cancer-related and all-cause mortality. The mechanisms of cancer-related muscle loss are multifactorial, including anorexia, hypogonadism, anaemia, inflammation, malnutrition, and aberrations in skeletal muscle protein turnover and metabolism.</p><p><strong>Methods: </strong>In this narrative review, we summarise relevant literature to (i) review the factors influencing skeletal muscle mass regulation, (ii) provide an overview of how cancer/treatments negatively impact these, (iii) review factors beyond muscle signalling that can impact the ability to participate in and respond to an exercise intervention to counteract muscle loss in cancer, and (iv) provide perspectives on critical areas of future research.</p><p><strong>Results: </strong>Despite the well-known benefits of exercise, there remains a paucity of clinical evidence supporting the impact of exercise in cancer-related muscle loss. There are numerous challenges to reversing muscle loss with exercise in clinical cancer settings, ranging from the impact of cancer/treatments on the molecular regulation of muscle mass, to clinical challenges in responsiveness to an exercise intervention. For example, tumour-related/treatment-related factors (e.g. nausea, pain, anaemia, and neutropenia), presence of comorbidities (e.g. diabetes, arthritis, and chronic obstructive pulmonary disease), injuries, disease progression and bone metastases, concomitant medications (e.g., metformin), can negatively affect an individual's ability to exercise safely and limit subsequent adaptation.</p><p><strong>Conclusions: </strong>This review identifies numerous gaps and oppportunities in the area of low muscle and muscle loss in cancer. Collaborative efforts between preclinical and clinical researchers are imperative to both understanding the mechanisms of atrophy, and develop appropriate therapeutic interventions.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":" ","pages":"52-67"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9481195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40367778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 8
Issue Information 问题信息
JCSM rapid communications Pub Date : 2022-01-01 DOI: 10.1002/rco2.42
{"title":"Issue Information","authors":"","doi":"10.1002/rco2.42","DOIUrl":"https://doi.org/10.1002/rco2.42","url":null,"abstract":"No abstract is available for this article.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47497999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Saturated fatty acids intake is associated with muscle atrophy in rheumatoid arthritis 饱和脂肪酸的摄入与类风湿关节炎的肌肉萎缩有关
JCSM rapid communications Pub Date : 2021-12-21 DOI: 10.1002/rco2.53
Mayu Sebe, R. Tsutsumi, Satoka Senoura, J. Kishi, Marina Iuchi, Yuna Mishima, Y. Tsutsumi, Masashi Kuroda, N. Harada, Y. Nakaya, Seizo Kinoshita, Y. Nishioka, H. Sakaue
{"title":"Saturated fatty acids intake is associated with muscle atrophy in rheumatoid arthritis","authors":"Mayu Sebe, R. Tsutsumi, Satoka Senoura, J. Kishi, Marina Iuchi, Yuna Mishima, Y. Tsutsumi, Masashi Kuroda, N. Harada, Y. Nakaya, Seizo Kinoshita, Y. Nishioka, H. Sakaue","doi":"10.1002/rco2.53","DOIUrl":"https://doi.org/10.1002/rco2.53","url":null,"abstract":"Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by joint inflammation, abnormal body composition, and an increased risk for sarcopenia. Muscle wasting in turn increases the risk of infection, morbidity, and premature mortality, but little is known of the relation between nutrient intake and sarcopenia in RA.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"101 - 86"},"PeriodicalIF":0.0,"publicationDate":"2021-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47424859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Voluntary exercise influences metastatic organotropism in a murine colorectal cancer model 自主运动影响小鼠结直肠癌模型的转移性器官倾向
JCSM rapid communications Pub Date : 2021-09-14 DOI: 10.1002/rco2.51
Liza A. Wijler, Daniëlle A. E. Raats, A. Verheem, A. Otter, H. Rundqvist, M. Dijk, A. May, O. Kranenburg
{"title":"Voluntary exercise influences metastatic organotropism in a murine colorectal cancer model","authors":"Liza A. Wijler, Daniëlle A. E. Raats, A. Verheem, A. Otter, H. Rundqvist, M. Dijk, A. May, O. Kranenburg","doi":"10.1002/rco2.51","DOIUrl":"https://doi.org/10.1002/rco2.51","url":null,"abstract":"Physical activity is associated with a lower risk of colorectal cancer (CRC) and CRC‐specific mortality. However, evidence for a causal relationship between physical activity and disease progression is lacking. Here, we have used CRC organoids to create a novel mouse model for spontaneous metastasis formation to multiple organs. We have used this model to assess the influence of voluntary exercise on disease progression.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"117 - 129"},"PeriodicalIF":0.0,"publicationDate":"2021-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/rco2.51","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49206019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Sarcopenia in young adults with congenital heart disease 青年先天性心脏病患者的肌萎缩
JCSM rapid communications Pub Date : 2021-09-10 DOI: 10.1002/rco2.49
Z. Khajali, Maryam Aliramezany, Fateme Jorfi, Homa Ghaderian, M. Maleki, H. Malek, S. Lotfian, Yasaman Khalili, N. Naderi
{"title":"Sarcopenia in young adults with congenital heart disease","authors":"Z. Khajali, Maryam Aliramezany, Fateme Jorfi, Homa Ghaderian, M. Maleki, H. Malek, S. Lotfian, Yasaman Khalili, N. Naderi","doi":"10.1002/rco2.49","DOIUrl":"https://doi.org/10.1002/rco2.49","url":null,"abstract":"The chronic nature of congenital heart diseases (CHDs) leads to the activation of inflammatory and neurohormonal processes in the body, and there is a possibility of the occurrence of other complications such as sarcopenia. The aim of the present study was to evaluate sarcopenia prevalence in adult patients with CHDs.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"77 - 85"},"PeriodicalIF":0.0,"publicationDate":"2021-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/rco2.49","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47632628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Mechanisms of chemotherapy‐induced muscle wasting in mice with cancer cachexia 癌症恶病质小鼠化疗诱导肌肉萎缩的机制
JCSM rapid communications Pub Date : 2021-08-26 DOI: 10.1002/rco2.50
K. Murphy, K. Swiderski, J. Ryall, J. Davey, H. Qian, S. Lamon, V. Foletta, J. Trieu, A. Chee, Suzannah J. Read, T. Naim, P. Gregorevic, G. Lynch
{"title":"Mechanisms of chemotherapy‐induced muscle wasting in mice with cancer cachexia","authors":"K. Murphy, K. Swiderski, J. Ryall, J. Davey, H. Qian, S. Lamon, V. Foletta, J. Trieu, A. Chee, Suzannah J. Read, T. Naim, P. Gregorevic, G. Lynch","doi":"10.1002/rco2.50","DOIUrl":"https://doi.org/10.1002/rco2.50","url":null,"abstract":"Cachexia is a debilitating complication of cancer characterized by progressive wasting and weakness of skeletal muscles that reduces quality of life and can compromise survival. Many anticancer treatments, such as chemotherapy, also cause muscle wasting, which impairs the response to treatment. Given that many cancer patients present with cachexia at the initiation of treatment, we investigated whether cachectic mice were susceptible to chemotherapy‐induced muscle wasting and to investigate contributing mechanisms, including the dysregulation of microRNAs (miRs).","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"102 - 116"},"PeriodicalIF":0.0,"publicationDate":"2021-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/rco2.50","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41931288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
The clinical significance of the calf circumference in non‐small‐cell lung cancer patients who undergo surgery 手术后非小细胞肺癌癌症患者小腿周长的临床意义
JCSM rapid communications Pub Date : 2021-08-24 DOI: 10.1002/rco2.48
Akihiro Nagoya, R. Kanzaki, K. Kimura, Eriko Fukui, T. Kanou, N. Ose, S. Funaki, M. Minami, Y. Shintani
{"title":"The clinical significance of the calf circumference in non‐small‐cell lung cancer patients who undergo surgery","authors":"Akihiro Nagoya, R. Kanzaki, K. Kimura, Eriko Fukui, T. Kanou, N. Ose, S. Funaki, M. Minami, Y. Shintani","doi":"10.1002/rco2.48","DOIUrl":"https://doi.org/10.1002/rco2.48","url":null,"abstract":"Calf circumference (CC), the greatest girth of the lower leg, is a simple tool for assessing sarcopenia. Its significance in patients with resectable non‐small‐cell lung cancer (NSCLC) is unknown.","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"5 1","pages":"40 - 51"},"PeriodicalIF":0.0,"publicationDate":"2021-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/rco2.48","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42864605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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