Pub Date : 2025-04-18DOI: 10.1016/j.isci.2025.112358
Marco J. Haenssgen , Tania Angeloff , Mark R. Herse , Elizabeth Auclair , Navaporn Sunanlikanon , Thipphaphone Xayavong , Jean-Marc Dubost , Somphavanh Radavanh , Chantho Vongnalath , Eric Deharo
International health organizations and experts and researchers from diverse fields consider the “One Health” concept (interdependence of human, animal, and environmental health) key to understanding global health security challenges such as the risk of pandemics from zoonotic disease emergence. However, the knowledge surrounding One Health retains critical blind spots for effective intervention design which we seek to address in this backstory article. We foreground lessons learned from an international workshop on everyday environmental heritage, held in Lao PDR in December 2024, to demonstrate the value of interdisciplinary and participatory exchanges for advancing the frontier of One Health scholarship and practice.
{"title":"Workshop report: Everyday environmental heritage is key to unlocking the social dimensions of One Health","authors":"Marco J. Haenssgen , Tania Angeloff , Mark R. Herse , Elizabeth Auclair , Navaporn Sunanlikanon , Thipphaphone Xayavong , Jean-Marc Dubost , Somphavanh Radavanh , Chantho Vongnalath , Eric Deharo","doi":"10.1016/j.isci.2025.112358","DOIUrl":"10.1016/j.isci.2025.112358","url":null,"abstract":"<div><div>International health organizations and experts and researchers from diverse fields consider the “One Health” concept (interdependence of human, animal, and environmental health) key to understanding global health security challenges such as the risk of pandemics from zoonotic disease emergence. However, the knowledge surrounding One Health retains critical blind spots for effective intervention design which we seek to address in this backstory article. We foreground lessons learned from an international workshop on everyday environmental heritage, held in Lao PDR in December 2024, to demonstrate the value of interdisciplinary and participatory exchanges for advancing the frontier of One Health scholarship and practice.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112358"},"PeriodicalIF":4.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-14DOI: 10.1016/j.isci.2025.112411
Reza Esmaillie, Michael Ignarski, Katrin Bohl, Tim Krüger, Daniyal Ahmad, Lisa Seufert, Bernhard Schermer, Thomas Benzing, Roman-Ulrich Müller, Francesca Fabretti
{"title":"Activation of Hypoxia-Inducible Factor Signaling Modulates the RNA Protein Interactome in Caenorhabditis elegans","authors":"Reza Esmaillie, Michael Ignarski, Katrin Bohl, Tim Krüger, Daniyal Ahmad, Lisa Seufert, Bernhard Schermer, Thomas Benzing, Roman-Ulrich Müller, Francesca Fabretti","doi":"10.1016/j.isci.2025.112411","DOIUrl":"10.1016/j.isci.2025.112411","url":null,"abstract":"","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112411"},"PeriodicalIF":4.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-11DOI: 10.1016/j.isci.2025.112400
Jaime Tan, Alicia Duron, Henry M. Sucov, Takako Makita
{"title":"Placode and neural crest origins of congenital deafness in mouse models of Waardenburg-Shah syndrome","authors":"Jaime Tan, Alicia Duron, Henry M. Sucov, Takako Makita","doi":"10.1016/j.isci.2025.112400","DOIUrl":"10.1016/j.isci.2025.112400","url":null,"abstract":"","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112400"},"PeriodicalIF":4.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143815840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-11DOI: 10.1016/j.isci.2025.112415
Magen N. Lord , Mai O. Spaulding , Jessica R. Hoffman , Rawad K. Basma , Emily E. Noble
Cannabinoid receptor agonists increase eating in a dose-dependent manner. However, the behavioral mechanisms by which cannabinoids modulate food intake control aren’t clear, particularly in females. We utilized a rodent model of cannabinoid administration modeling a common route of cannabinoid consumption in humans: edibles. Herein, we administered the dual cannabinoid receptor agonist CP55940 in edible form to female rats and observed acute increases in standard chow intake due to an increase in meal size with no change in meal number. We further observed that the hyperphagic dose of edible CP55940 increases impulsive responding for sucrose, but this did not coincide with changes in motivation for sucrose. Finally, cannabinoids can affect anxiety-like behavior, but the acutely hyperphagic dose used in our studies had no effect on anxiety-like behavior. We conclude that edible cannabinoid administration delays satiation and increases impulsive eating behavior without impacting food motivation, potentially by reducing inhibitory control.
{"title":"Edible cannabinoids impact meal structure and food impulsivity in female rats","authors":"Magen N. Lord , Mai O. Spaulding , Jessica R. Hoffman , Rawad K. Basma , Emily E. Noble","doi":"10.1016/j.isci.2025.112415","DOIUrl":"10.1016/j.isci.2025.112415","url":null,"abstract":"<div><div>Cannabinoid receptor agonists increase eating in a dose-dependent manner. However, the behavioral mechanisms by which cannabinoids modulate food intake control aren’t clear, particularly in females. We utilized a rodent model of cannabinoid administration modeling a common route of cannabinoid consumption in humans: edibles. Herein, we administered the dual cannabinoid receptor agonist CP55940 in edible form to female rats and observed acute increases in standard chow intake due to an increase in meal size with no change in meal number. We further observed that the hyperphagic dose of edible CP55940 increases impulsive responding for sucrose, but this did not coincide with changes in motivation for sucrose. Finally, cannabinoids can affect anxiety-like behavior, but the acutely hyperphagic dose used in our studies had no effect on anxiety-like behavior. We conclude that edible cannabinoid administration delays satiation and increases impulsive eating behavior without impacting food motivation, potentially by reducing inhibitory control.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112415"},"PeriodicalIF":4.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-10DOI: 10.1016/j.isci.2025.112403
Selami Baglamis , Vivek M. Sheraton , Sanne M. van Neerven , Adrian Logiantara , Lisanne E. Nijman , Laura A. Hageman , Nicolas Léveillé , Clara C. Elbers , Maarten F. Bijlsma , Louis Vermeulen , Przemek M. Krawczyk , Kristiaan J. Lenos
Clonal dispersal, resulting from the intermingling of tumor cell subpopulations, is thought to be a key driver of tumor heterogeneity. Despite advances in spatial modeling of cancer biology, quantification of clonal dispersal has been challenging. This study introduces a straightforward method, relying on fluorescent cell barcoding, to quantify clonal dispersal in various in vitro and in vivo models of colorectal cancer (CRC). Our approach allows for precise localization of clones and uncovering the degree of clonal mixing across different CRC models. Our findings suggest that clonal dispersal is correlated with the expression of genes involved in epithelial-mesenchymal transition and CMS4-related signaling pathways. We further identify a dispersal gene signature, associated with intratumor heterogeneity, which is a robust clinical predictor of poor prognosis and recurrence in CRC, highlighting its potential as a prognostic marker and a putative direction for therapeutic targeting.
{"title":"Clonal dispersal is associated with tumor heterogeneity and poor prognosis in colorectal cancer","authors":"Selami Baglamis , Vivek M. Sheraton , Sanne M. van Neerven , Adrian Logiantara , Lisanne E. Nijman , Laura A. Hageman , Nicolas Léveillé , Clara C. Elbers , Maarten F. Bijlsma , Louis Vermeulen , Przemek M. Krawczyk , Kristiaan J. Lenos","doi":"10.1016/j.isci.2025.112403","DOIUrl":"10.1016/j.isci.2025.112403","url":null,"abstract":"<div><div>Clonal dispersal, resulting from the intermingling of tumor cell subpopulations, is thought to be a key driver of tumor heterogeneity. Despite advances in spatial modeling of cancer biology, quantification of clonal dispersal has been challenging. This study introduces a straightforward method, relying on fluorescent cell barcoding, to quantify clonal dispersal in various <em>in vitro</em> and <em>in vivo</em> models of colorectal cancer (CRC). Our approach allows for precise localization of clones and uncovering the degree of clonal mixing across different CRC models. Our findings suggest that clonal dispersal is correlated with the expression of genes involved in epithelial-mesenchymal transition and CMS4-related signaling pathways. We further identify a dispersal gene signature, associated with intratumor heterogeneity, which is a robust clinical predictor of poor prognosis and recurrence in CRC, highlighting its potential as a prognostic marker and a putative direction for therapeutic targeting.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112403"},"PeriodicalIF":4.6,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-10DOI: 10.1016/j.isci.2025.112398
Na Qu , Abdelkader Daoud , Daniel O. Kechele , Cassie E. Cleary , Jorge O. Múnera
The cloaca is a transient structure that forms in the terminal hindgut giving rise to the rectum dorsally and the urogenital sinus ventrally. Similarly, human hindgut cultures derived from human pluripotent stem cells generate human colonic organoids (HCOs) which also contain co-developing urothelial tissue. In this study, our goal was to identify pathways involved in cloacal patterning and apply this to human hindgut cultures. RNA sequencing (RNA-seq) data comparing dorsal versus ventral cloaca in e10.5 mice revealed that WNT signaling was elevated in the ventral versus dorsal cloaca. Inhibition of WNT signaling in hindgut cultures maintained their differentiation toward colonic organoids. WNT activation promoted differentiation toward human urothelial organoids (HUOs). HUOs contained developmental stage specific cell types present in mammalian urothelial tissue including co-developing mesenchyme. Therefore, HUOs offer a powerful in vitro model for dissecting the regulatory pathways that control the dynamic emergence of stage specific cell types within the human urothelium.
{"title":"Differentiation of human pluripotent stem cells into urothelial organoids via transient activation of WNT signaling","authors":"Na Qu , Abdelkader Daoud , Daniel O. Kechele , Cassie E. Cleary , Jorge O. Múnera","doi":"10.1016/j.isci.2025.112398","DOIUrl":"10.1016/j.isci.2025.112398","url":null,"abstract":"<div><div>The cloaca is a transient structure that forms in the terminal hindgut giving rise to the rectum dorsally and the urogenital sinus ventrally. Similarly, human hindgut cultures derived from human pluripotent stem cells generate human colonic organoids (HCOs) which also contain co-developing urothelial tissue. In this study, our goal was to identify pathways involved in cloacal patterning and apply this to human hindgut cultures. RNA sequencing (RNA-seq) data comparing dorsal versus ventral cloaca in e10.5 mice revealed that WNT signaling was elevated in the ventral versus dorsal cloaca. Inhibition of WNT signaling in hindgut cultures maintained their differentiation toward colonic organoids. WNT activation promoted differentiation toward human urothelial organoids (HUOs). HUOs contained developmental stage specific cell types present in mammalian urothelial tissue including co-developing mesenchyme. Therefore, HUOs offer a powerful <em>in vitro</em> model for dissecting the regulatory pathways that control the dynamic emergence of stage specific cell types within the human urothelium.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112398"},"PeriodicalIF":4.6,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143859755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-09DOI: 10.1016/j.isci.2025.112363
Kuan Yoow Chan , Yini Yu , Yidi Kong , Ling Cheng , Renzhi Yao , Phoebe Sha Yin Chair , Ping Wang , Rong Wang , Wan-Yang Sun , Rong-Rong He , Junxia Min , Fudi Wang , Mikael Björklund
Despite wide variation, each cell type has an optimal size. Maintaining optimal size is essential for cellular fitness and function but the biological basis for this remains elusive. Here, we performed fitness analysis involving genome-wide CRISPR-Cas9 knockout data from tens of human cell lines and identified that cell size influences the essentiality of genes related to mitochondria and membrane repair. These genes also included glutathione peroxidase 4 (GPX4), which safeguards membranes from oxidative damage and prevents ferroptosis—iron-dependent death. Growth beyond normal size, with or without cell-cycle arrest, increased lipid peroxidation, resulting in a ferroptosis-sensitive state. Proteomic analysis revealed cell-cycle-independent superscaling of endoplasmic reticulum, accumulation of iron, and lipidome remodeling. Even slight increases from normal cell size sensitized proliferating cells to ferroptosis as evidenced by deep-learning-based single-cell analysis. Thus, lipid peroxidation may be a fitness trade-off that constrains cell enlargement and contributes to the establishment of an optimal cell size.
{"title":"GPX4-dependent ferroptosis sensitivity is a fitness trade-off for cell enlargement","authors":"Kuan Yoow Chan , Yini Yu , Yidi Kong , Ling Cheng , Renzhi Yao , Phoebe Sha Yin Chair , Ping Wang , Rong Wang , Wan-Yang Sun , Rong-Rong He , Junxia Min , Fudi Wang , Mikael Björklund","doi":"10.1016/j.isci.2025.112363","DOIUrl":"10.1016/j.isci.2025.112363","url":null,"abstract":"<div><div>Despite wide variation, each cell type has an optimal size. Maintaining optimal size is essential for cellular fitness and function but the biological basis for this remains elusive. Here, we performed fitness analysis involving genome-wide CRISPR-Cas9 knockout data from tens of human cell lines and identified that cell size influences the essentiality of genes related to mitochondria and membrane repair. These genes also included glutathione peroxidase 4 (GPX4), which safeguards membranes from oxidative damage and prevents ferroptosis—iron-dependent death. Growth beyond normal size, with or without cell-cycle arrest, increased lipid peroxidation, resulting in a ferroptosis-sensitive state. Proteomic analysis revealed cell-cycle-independent superscaling of endoplasmic reticulum, accumulation of iron, and lipidome remodeling. Even slight increases from normal cell size sensitized proliferating cells to ferroptosis as evidenced by deep-learning-based single-cell analysis. Thus, lipid peroxidation may be a fitness trade-off that constrains cell enlargement and contributes to the establishment of an optimal cell size.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112363"},"PeriodicalIF":4.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143854424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-08DOI: 10.1016/j.isci.2025.112369
Yi Liu , Xiaojing Liu , Ruishan Liu , Hao Xu , Mantao Chen , Jiajie Qian , Beiwen Zheng
Carbapenem-resistant Enterobacteriaceae (CRE) have emerged as a critical threat to global health, and multicopy resistance genes are a potential contributor to increased resistance. This study investigates a novel arrangement of four blaNDM-1 genes in tandem on an IncFII plasmid from Enterobacter hormaechei. Whole-genome sequencing (WGS) of E. hormaechei isolates L710hy identified a four-tandem repeat of the blaNDM-1 gene, with each copy’s environment nearly identical (ISCR1-aph(3′)-VI-ISAba125-blaNDM-1-ble-iso-tat-dsbD-cutA-sul1-ISCR1). The study suggests a correlation between the blaNDM-1 copy number and minimum inhibitory concentration (MIC) values for carbapenems, though further research is needed to confirm this correlation. The stability of these four blaNDM-1 tandem repeat structures was also investigated. This is the first documented case of blaNDM-1 tandem repeats in E. hormaechei, and the ISCR1 and other insertion sequence may play a role in this arrangement.
{"title":"First characterization of four repeat regions with the blaNDM-1 carried on an IncFII plasmid in Enterobacter hormaechei","authors":"Yi Liu , Xiaojing Liu , Ruishan Liu , Hao Xu , Mantao Chen , Jiajie Qian , Beiwen Zheng","doi":"10.1016/j.isci.2025.112369","DOIUrl":"10.1016/j.isci.2025.112369","url":null,"abstract":"<div><div>Carbapenem-resistant Enterobacteriaceae (CRE) have emerged as a critical threat to global health, and multicopy resistance genes are a potential contributor to increased resistance. This study investigates a novel arrangement of four <em>bla</em><sub>NDM-1</sub> genes in tandem on an IncFII plasmid from <em>Enterobacter hormaechei</em>. Whole-genome sequencing (WGS) of <em>E. hormaechei</em> isolates L710hy identified a four-tandem repeat of the <em>bla</em><sub>NDM-1</sub> gene, with each copy’s environment nearly identical (IS<em>CR1</em>-<em>aph(3′)-VI</em>-IS<em>Aba125</em>-<em>bla</em><sub>NDM-1</sub>-<em>ble</em>-<em>iso</em>-<em>tat</em>-<em>dsbD</em>-<em>cutA</em>-<em>sul1</em>-IS<em>CR1</em>). The study suggests a correlation between the <em>bla</em><sub>NDM-1</sub> copy number and minimum inhibitory concentration (MIC) values for carbapenems, though further research is needed to confirm this correlation. The stability of these four <em>bla</em><sub>NDM-1</sub> tandem repeat structures was also investigated. This is the first documented case of <em>bla</em><sub>NDM-1</sub> tandem repeats in <em>E. hormaechei</em>, and the IS<em>CR1</em> and other insertion sequence may play a role in this arrangement.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112369"},"PeriodicalIF":4.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143854705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-08DOI: 10.1016/j.isci.2025.112371
Feng He , Ralph M. Nichols , Melina A. Agosto , Theodore G. Wensel
Phosphatidylinositol-3-phosphate (PI(3)P) is important for multiple functions of retinal pigmented epithelial (RPE) cells, but its functions in RPE have not been studied. In RPE from mouse eyes and in cultured human RPE cells, PI(3)P-enriched membranes include endosomes, the trans-Golgi network, phagosomes, and autophagophores. Mouse RPE cells lacking activity of the PI-3 kinase, Vps34, lack detectable PI(3)P and die prematurely. Phagosomes containing rod discs accumulate, as do membrane aggregates positive for autophagosome markers. These autophagy-related membranes recruit LC3/Atg8 without Vps34, but phagosomes do not. Vps34 loss leads to accumulation of lysosomes which do not fuse with phagosomes or membranes with autophagy markers. Thus, Vps34-derived PI(3)P is not needed for initiation of phagocytosis or endocytosis, nor for formation of membranes containing autophagy markers. In contrast, Vps34 and PI(3)P are essential for intermediate and later stages, including membrane fusion with lysosomes.
{"title":"Roles of class III phosphatidylinositol 3-kinase, Vps34, in phagocytosis, autophagy, and endocytosis in retinal pigmented epithelium","authors":"Feng He , Ralph M. Nichols , Melina A. Agosto , Theodore G. Wensel","doi":"10.1016/j.isci.2025.112371","DOIUrl":"10.1016/j.isci.2025.112371","url":null,"abstract":"<div><div>Phosphatidylinositol-3-phosphate (PI(3)P) is important for multiple functions of retinal pigmented epithelial (RPE) cells, but its functions in RPE have not been studied. In RPE from mouse eyes and in cultured human RPE cells, PI(3)P-enriched membranes include endosomes, the <em>trans-</em>Golgi network, phagosomes, and autophagophores. Mouse RPE cells lacking activity of the PI-3 kinase, Vps34, lack detectable PI(3)P and die prematurely. Phagosomes containing rod discs accumulate, as do membrane aggregates positive for autophagosome markers. These autophagy-related membranes recruit LC3/Atg8 without Vps34, but phagosomes do not. Vps34 loss leads to accumulation of lysosomes which do not fuse with phagosomes or membranes with autophagy markers. Thus, Vps34-derived PI(3)P is not needed for initiation of phagocytosis or endocytosis, nor for formation of membranes containing autophagy markers. In contrast, Vps34 and PI(3)P are essential for intermediate and later stages, including membrane fusion with lysosomes.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"28 5","pages":"Article 112371"},"PeriodicalIF":4.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143854707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号