Pub Date : 2024-11-22DOI: 10.1038/s42255-024-01169-7
Mhairi Paul, Mark Nixon
Cushing’s syndrome, a condition of chronic glucocorticoid excess, disrupts metabolic homeostasis, driving fat redistribution and promoting insulin resistance. New research uses a series of elegant approaches to reveal acyl-CoA-binding protein (ACBP) as a mediator of the metabolic disturbances associated with elevated glucocorticoid levels in mice.
{"title":"ACBP orchestrates the metabolic phenotype in Cushing’s syndrome","authors":"Mhairi Paul, Mark Nixon","doi":"10.1038/s42255-024-01169-7","DOIUrl":"10.1038/s42255-024-01169-7","url":null,"abstract":"Cushing’s syndrome, a condition of chronic glucocorticoid excess, disrupts metabolic homeostasis, driving fat redistribution and promoting insulin resistance. New research uses a series of elegant approaches to reveal acyl-CoA-binding protein (ACBP) as a mediator of the metabolic disturbances associated with elevated glucocorticoid levels in mice.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 12","pages":"2220-2221"},"PeriodicalIF":18.9,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142684158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-22DOI: 10.1038/s42255-024-01167-9
Mauricio Berriel Diaz, Maria Rohm, Stephan Herzig
Cancer cachexia is a complex metabolic disorder marked by unintentional body weight loss or ‘wasting’ of body mass, driven by multiple aetiological factors operating at various levels. It is associated with many malignancies and significantly contributes to cancer-related morbidity and mortality. With emerging recognition of cancer as a systemic disease, there is increasing awareness that understanding and treatment of cancer cachexia may represent a crucial cornerstone for improved management of cancer. Here, we describe the metabolic changes contributing to body wasting in cachexia and explain how the entangled action of both tumour-derived and host-amplified processes induces these metabolic changes. We discuss energy homeostasis and possible ways that the presence of a tumour interferes with or hijacks physiological energy conservation pathways. In that context, we highlight the role played by metabolic cross-talk mechanisms in cachexia pathogenesis. Lastly, we elaborate on the challenges and opportunities in the treatment of this devastating paraneoplastic phenomenon that arise from the complex and multifaceted metabolic cross-talk mechanisms and provide a status on current and emerging therapeutic approaches. In this Review, the authors highlight cancer cachexia as a complex and multifactorial disorder, and discuss the underlying host-driven and tumour-driven metabolic changes, therapeutic opportunities and the pertinent challenges in the treatment of cancer cachexia.
{"title":"Cancer cachexia: multilevel metabolic dysfunction","authors":"Mauricio Berriel Diaz, Maria Rohm, Stephan Herzig","doi":"10.1038/s42255-024-01167-9","DOIUrl":"10.1038/s42255-024-01167-9","url":null,"abstract":"Cancer cachexia is a complex metabolic disorder marked by unintentional body weight loss or ‘wasting’ of body mass, driven by multiple aetiological factors operating at various levels. It is associated with many malignancies and significantly contributes to cancer-related morbidity and mortality. With emerging recognition of cancer as a systemic disease, there is increasing awareness that understanding and treatment of cancer cachexia may represent a crucial cornerstone for improved management of cancer. Here, we describe the metabolic changes contributing to body wasting in cachexia and explain how the entangled action of both tumour-derived and host-amplified processes induces these metabolic changes. We discuss energy homeostasis and possible ways that the presence of a tumour interferes with or hijacks physiological energy conservation pathways. In that context, we highlight the role played by metabolic cross-talk mechanisms in cachexia pathogenesis. Lastly, we elaborate on the challenges and opportunities in the treatment of this devastating paraneoplastic phenomenon that arise from the complex and multifaceted metabolic cross-talk mechanisms and provide a status on current and emerging therapeutic approaches. In this Review, the authors highlight cancer cachexia as a complex and multifactorial disorder, and discuss the underlying host-driven and tumour-driven metabolic changes, therapeutic opportunities and the pertinent challenges in the treatment of cancer cachexia.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 12","pages":"2222-2245"},"PeriodicalIF":18.9,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142684163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-21DOI: 10.1038/s42255-024-01162-0
Shu Feng, Na Xie, Yongzhen Liu, Chao Qin, Ali Can Savas, Ting-Yu Wang, Shutong Li, Youliang Rao, Alexandra Shambayate, Tsui-Fen Chou, Charles Brenner, Canhua Huang, Pinghui Feng
As obligate intracellular pathogens, viruses activate host metabolic enzymes to supply intermediates that support progeny production. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of salvage nicotinamide adenine dinucleotide (NAD+) synthesis, is an interferon-inducible protein that inhibits the replication of several RNA and DNA viruses through unknown mechanisms. Here, we show that NAMPT restricts herpes simplex virus type 1 (HSV-1) replication by impeding the virion incorporation of viral proteins owing to its phosphoribosyl-hydrolase (phosphoribosylase) activity, which is independent of the role of NAMPT in NAD+ synthesis. Proteomics analysis of HSV-1-infected cells identifies phosphoribosylated viral structural proteins, particularly glycoproteins and tegument proteins, which are de-phosphoribosylated by NAMPT in vitro and in cells. Chimeric and recombinant HSV-1 carrying phosphoribosylation-resistant mutations show that phosphoribosylation promotes the incorporation of structural proteins into HSV-1 virions and subsequent virus entry. Loss of NAMPT renders mice highly susceptible to HSV-1 infection. Our work describes an additional enzymatic activity of a metabolic enzyme in viral infection and host defence, offering a system to interrogate the roles of protein phosphoribosylation in metazoans. The NAD+ synthesis enzyme NAMPT is shown to possess additional enzymatic activity as a phosphoribosylase, which restricts the virion incorporation of viral proteins and underpins its antiviral effect
{"title":"Cryptic phosphoribosylase activity of NAMPT restricts the virion incorporation of viral proteins","authors":"Shu Feng, Na Xie, Yongzhen Liu, Chao Qin, Ali Can Savas, Ting-Yu Wang, Shutong Li, Youliang Rao, Alexandra Shambayate, Tsui-Fen Chou, Charles Brenner, Canhua Huang, Pinghui Feng","doi":"10.1038/s42255-024-01162-0","DOIUrl":"10.1038/s42255-024-01162-0","url":null,"abstract":"As obligate intracellular pathogens, viruses activate host metabolic enzymes to supply intermediates that support progeny production. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of salvage nicotinamide adenine dinucleotide (NAD+) synthesis, is an interferon-inducible protein that inhibits the replication of several RNA and DNA viruses through unknown mechanisms. Here, we show that NAMPT restricts herpes simplex virus type 1 (HSV-1) replication by impeding the virion incorporation of viral proteins owing to its phosphoribosyl-hydrolase (phosphoribosylase) activity, which is independent of the role of NAMPT in NAD+ synthesis. Proteomics analysis of HSV-1-infected cells identifies phosphoribosylated viral structural proteins, particularly glycoproteins and tegument proteins, which are de-phosphoribosylated by NAMPT in vitro and in cells. Chimeric and recombinant HSV-1 carrying phosphoribosylation-resistant mutations show that phosphoribosylation promotes the incorporation of structural proteins into HSV-1 virions and subsequent virus entry. Loss of NAMPT renders mice highly susceptible to HSV-1 infection. Our work describes an additional enzymatic activity of a metabolic enzyme in viral infection and host defence, offering a system to interrogate the roles of protein phosphoribosylation in metazoans. The NAD+ synthesis enzyme NAMPT is shown to possess additional enzymatic activity as a phosphoribosylase, which restricts the virion incorporation of viral proteins and underpins its antiviral effect","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 12","pages":"2300-2318"},"PeriodicalIF":18.9,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-20DOI: 10.1038/s42255-024-01158-w
Despite their abundance and despite being the most numerous biological entities on Earth, viruses remain one of the least understood components of the human microbiome. In our study, we show how Microviridae bacteriophages in the gut microbiome are associated with food addiction through changes in tryptophan, serotonin and dopamine metabolism.
{"title":"Microviridae bacteriophages in the gut microbiome and food addiction in humans","authors":"","doi":"10.1038/s42255-024-01158-w","DOIUrl":"10.1038/s42255-024-01158-w","url":null,"abstract":"Despite their abundance and despite being the most numerous biological entities on Earth, viruses remain one of the least understood components of the human microbiome. In our study, we show how Microviridae bacteriophages in the gut microbiome are associated with food addiction through changes in tryptophan, serotonin and dopamine metabolism.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 11","pages":"2035-2036"},"PeriodicalIF":18.9,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142673926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-11DOI: 10.1038/s42255-024-01163-z
Qian Gao, Zhiwei Tang, Haili Wang, Maya Yamazaki, Jia Jiang, Ying-Hui Fu, Louis J. Ptacek, Luoying Zhang
Our brain adapts to seasonal changes. Mis-adaptations may lead to seasonal patterns in several psychiatric disorders, but we know little regarding the underlying mechanisms. Our previous work identified two variants in the human circadian clock gene PERIOD3 (PER3), that is, P415A and H417R, which are associated with winter depression, but whether and how these variants lead to the disorder remain to be characterized. Here we find that male mice carrying human P415A and H417R display winter depression-like behaviours that are caused by the actions of P415A and H417R in the adrenal gland. Systemic corticosterone level is downregulated in adaptation to shortening of day length, while P415A and H417R eliminate this downregulation by increasing corticosterone synthesis. Enhanced glucocorticoid signalling represses the transcription of Tph2, which encodes the rate-limiting enzyme of serotonin synthesis, leading to increased depression-like behaviours. Taken together, our findings unveil a mechanism according to which human variants contribute to seasonal mood traits. The authors show how genetic variants of the human circadian clock gene PER3 are related to winter depression. In mice, under shorter light exposure, such variants enhance glucocorticoid signalling, inhibiting serotonin production and leading to depression-like behaviours.
{"title":"Human PERIOD3 variants lead to winter depression-like behaviours via glucocorticoid signalling","authors":"Qian Gao, Zhiwei Tang, Haili Wang, Maya Yamazaki, Jia Jiang, Ying-Hui Fu, Louis J. Ptacek, Luoying Zhang","doi":"10.1038/s42255-024-01163-z","DOIUrl":"10.1038/s42255-024-01163-z","url":null,"abstract":"Our brain adapts to seasonal changes. Mis-adaptations may lead to seasonal patterns in several psychiatric disorders, but we know little regarding the underlying mechanisms. Our previous work identified two variants in the human circadian clock gene PERIOD3 (PER3), that is, P415A and H417R, which are associated with winter depression, but whether and how these variants lead to the disorder remain to be characterized. Here we find that male mice carrying human P415A and H417R display winter depression-like behaviours that are caused by the actions of P415A and H417R in the adrenal gland. Systemic corticosterone level is downregulated in adaptation to shortening of day length, while P415A and H417R eliminate this downregulation by increasing corticosterone synthesis. Enhanced glucocorticoid signalling represses the transcription of Tph2, which encodes the rate-limiting enzyme of serotonin synthesis, leading to increased depression-like behaviours. Taken together, our findings unveil a mechanism according to which human variants contribute to seasonal mood traits. The authors show how genetic variants of the human circadian clock gene PER3 are related to winter depression. In mice, under shorter light exposure, such variants enhance glucocorticoid signalling, inhibiting serotonin production and leading to depression-like behaviours.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 12","pages":"2267-2280"},"PeriodicalIF":18.9,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142597982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-08DOI: 10.1038/s42255-024-01165-x
AI-READI Consortium
Here, we introduce Artificial Intelligence Ready and Equitable Atlas for Diabetes Insights (AI-READI), a multidisciplinary data-generation project designed to create and share a multimodal dataset optimized for artificial intelligence research in type 2 diabetes mellitus.
{"title":"AI-READI: rethinking AI data collection, preparation and sharing in diabetes research and beyond","authors":"AI-READI Consortium","doi":"10.1038/s42255-024-01165-x","DOIUrl":"10.1038/s42255-024-01165-x","url":null,"abstract":"Here, we introduce Artificial Intelligence Ready and Equitable Atlas for Diabetes Insights (AI-READI), a multidisciplinary data-generation project designed to create and share a multimodal dataset optimized for artificial intelligence research in type 2 diabetes mellitus.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 12","pages":"2210-2212"},"PeriodicalIF":18.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142597489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-05DOI: 10.1038/s42255-024-01171-z
Wusheng Xiao, Nishith Shrimali, Niv Vigder, William M. Oldham, Clary B. Clish, Huamei He, Samantha J. Wong, Bradley M. Wertheim, Elena Arons, Marcia C. Haigis, Jane A. Leopold, Joseph Loscalzo
{"title":"Author Correction: Branched-chain α-ketoacids aerobically activate HIF1α signalling in vascular cells","authors":"Wusheng Xiao, Nishith Shrimali, Niv Vigder, William M. Oldham, Clary B. Clish, Huamei He, Samantha J. Wong, Bradley M. Wertheim, Elena Arons, Marcia C. Haigis, Jane A. Leopold, Joseph Loscalzo","doi":"10.1038/s42255-024-01171-z","DOIUrl":"10.1038/s42255-024-01171-z","url":null,"abstract":"","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 11","pages":"2203-2203"},"PeriodicalIF":18.9,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s42255-024-01171-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-04DOI: 10.1038/s42255-024-01159-9
Sorabh Sharma, Manjinder Cheema, Patrick L. Reeson, Kamal Narayana, Roobina Boghozian, Ana Paula Cota, Tara P. Brosschot, Rachael D. FitzPatrick, Jakob Körbelin, Lisa A. Reynolds, Craig E. Brown
Vascular pathology is associated with cognitive impairment in diseases such as type 1 diabetes; however, how capillary flow is affected and the underlying mechanisms remain elusive. Here we show that capillaries in the diabetic mouse brain in both sexes are prone to stalling, with blocks consisting primarily of erythrocytes in branches off ascending venules. Screening for circulating inflammatory cytokines revealed persistently high levels of interleukin-10 (IL-10) in diabetic mice. Contrary to expectation, stimulating IL-10 signalling increased capillary obstruction, whereas inhibiting IL-10 receptors with neutralizing antibodies or endothelial specific knockdown in diabetic mice reversed these impairments. Chronic treatment of diabetic mice with IL-10 receptor neutralizing antibodies improved cerebral blood flow, increased capillary flux and diameter, downregulated haemostasis and cell adhesion-related gene expression, and reversed cognitive deficits. These data suggest that IL-10 signalling has an unexpected pathogenic role in cerebral microcirculatory defects and cognitive impairment associated with type 1 diabetes. Interleukin-10 promotes the formation of microcirculatory defects in the brain associated with cognitive impairment in a mouse model of type 1 diabetes.
{"title":"A pathogenic role for IL-10 signalling in capillary stalling and cognitive impairment in type 1 diabetes","authors":"Sorabh Sharma, Manjinder Cheema, Patrick L. Reeson, Kamal Narayana, Roobina Boghozian, Ana Paula Cota, Tara P. Brosschot, Rachael D. FitzPatrick, Jakob Körbelin, Lisa A. Reynolds, Craig E. Brown","doi":"10.1038/s42255-024-01159-9","DOIUrl":"10.1038/s42255-024-01159-9","url":null,"abstract":"Vascular pathology is associated with cognitive impairment in diseases such as type 1 diabetes; however, how capillary flow is affected and the underlying mechanisms remain elusive. Here we show that capillaries in the diabetic mouse brain in both sexes are prone to stalling, with blocks consisting primarily of erythrocytes in branches off ascending venules. Screening for circulating inflammatory cytokines revealed persistently high levels of interleukin-10 (IL-10) in diabetic mice. Contrary to expectation, stimulating IL-10 signalling increased capillary obstruction, whereas inhibiting IL-10 receptors with neutralizing antibodies or endothelial specific knockdown in diabetic mice reversed these impairments. Chronic treatment of diabetic mice with IL-10 receptor neutralizing antibodies improved cerebral blood flow, increased capillary flux and diameter, downregulated haemostasis and cell adhesion-related gene expression, and reversed cognitive deficits. These data suggest that IL-10 signalling has an unexpected pathogenic role in cerebral microcirculatory defects and cognitive impairment associated with type 1 diabetes. Interleukin-10 promotes the formation of microcirculatory defects in the brain associated with cognitive impairment in a mouse model of type 1 diabetes.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 11","pages":"2082-2099"},"PeriodicalIF":18.9,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s42255-024-01159-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142574461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-04DOI: 10.1038/s42255-024-01161-1
Celine E. Riera
A new study finds that capillary vessels become obstructed in diabetes and that their dysfunction may cause microvascular damage and lead to cognitive deficits. Such obstruction is independent of the elevated blood sugar found in diabetes and is triggered by elevated interleukin-10 cytokine signalling in cerebral blood vessel endothelial cells.
{"title":"Diabetes, IL-10 and the brain’s microvascular crisis","authors":"Celine E. Riera","doi":"10.1038/s42255-024-01161-1","DOIUrl":"10.1038/s42255-024-01161-1","url":null,"abstract":"A new study finds that capillary vessels become obstructed in diabetes and that their dysfunction may cause microvascular damage and lead to cognitive deficits. Such obstruction is independent of the elevated blood sugar found in diabetes and is triggered by elevated interleukin-10 cytokine signalling in cerebral blood vessel endothelial cells.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 11","pages":"2029-2030"},"PeriodicalIF":18.9,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142574460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-31DOI: 10.1038/s42255-024-01116-6
Leslie J. Baier, Clifton Bogardus
A nonsense mutation in TBC1D4 has previously been associated with hyperinsulinaemia and increased risk of type 2 diabetes mellitus. A new report shows that carriers have isolated muscle insulin resistance that improves after an acute bout of exercise.
{"title":"Effect of acute exercise in carriers of TBC1D4 mutation","authors":"Leslie J. Baier, Clifton Bogardus","doi":"10.1038/s42255-024-01116-6","DOIUrl":"10.1038/s42255-024-01116-6","url":null,"abstract":"A nonsense mutation in TBC1D4 has previously been associated with hyperinsulinaemia and increased risk of type 2 diabetes mellitus. A new report shows that carriers have isolated muscle insulin resistance that improves after an acute bout of exercise.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"6 12","pages":"2213-2214"},"PeriodicalIF":18.9,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142555818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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