American journal of physiology. Cell physiology最新文献

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Melatonin mitigates matrix stiffness-induced disc degenetation by inhibiting reactive oxygen species and melatonin receptor mediated-PI3K/AKT/NF-κB pathway 褪黑激素通过抑制活性氧和褪黑激素受体介导的PI3K/AKT/NF-κB通路,减轻基质僵化诱发的椎间盘退化
IF 5.5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00630.2023
Zhihui Liang, Jia Song, Wen-ji Shangguan, Qiu-qi Zhang, Jiang Shao, Yue-hui Zhang
{"title":"Melatonin mitigates matrix stiffness-induced disc degenetation by inhibiting reactive oxygen species and melatonin receptor mediated-PI3K/AKT/NF-κB pathway","authors":"Zhihui Liang, Jia Song, Wen-ji Shangguan, Qiu-qi Zhang, Jiang Shao, Yue-hui Zhang","doi":"10.1152/ajpcell.00630.2023","DOIUrl":"https://doi.org/10.1152/ajpcell.00630.2023","url":null,"abstract":"American Journal of Physiology-Cell Physiology, Ahead of Print. <br/>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"15 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142204163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Corrigendum for Hagen et al., volume 327, 2024, p. C372–C378 Hagen 等人的更正,第 327 卷,2024 年,第 C372-C378 页
IF 5.5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-09 DOI: 10.1152/ajpcell.00326.2024_cor
{"title":"Corrigendum for Hagen et al., volume 327, 2024, p. C372–C378","authors":"","doi":"10.1152/ajpcell.00326.2024_cor","DOIUrl":"https://doi.org/10.1152/ajpcell.00326.2024_cor","url":null,"abstract":"American Journal of Physiology-Cell Physiology, Volume 327, Issue 3, Page C867-C867, September 2024. <br/>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"14 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142204250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Involvement of the gut microbiota in cancer cachexia. 肠道微生物群对癌症恶病质的影响
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-09 DOI: 10.1152/ajpcell.00327.2024
Brandon N VanderVeen, Thomas D Cardaci, Brooke M Bullard, Michael Madden, Jie Li, Kandy T Velazquez, Jason L Kubinak, Daping Fan, E Angela Murphy
{"title":"Involvement of the gut microbiota in cancer cachexia.","authors":"Brandon N VanderVeen, Thomas D Cardaci, Brooke M Bullard, Michael Madden, Jie Li, Kandy T Velazquez, Jason L Kubinak, Daping Fan, E Angela Murphy","doi":"10.1152/ajpcell.00327.2024","DOIUrl":"10.1152/ajpcell.00327.2024","url":null,"abstract":"<p><p>Cancer cachexia, or the unintentional loss of body weight in patients with cancer, is a multiorgan and multifactorial syndrome with a complex and largely unknown etiology; however, metabolic dysfunction and inflammation remain hallmarks of cancer-associated wasting. Although cachexia manifests with muscle and adipose tissue loss, perturbations to the gastrointestinal tract may serve as the frontline for both impaired nutrient absorption and immune-activating gut dysbiosis. Investigations into the gut microbiota have exploded within the past two decades, demonstrating multiple gut-tissue axes; however, the link between adipose and skeletal muscle wasting and the gut microbiota with cancer is only beginning to be understood. Furthermore, the most used anticancer drugs (e.g. chemotherapy and immune checkpoint inhibitors) negatively impact gut homeostasis, potentially exacerbating wasting and contributing to poor patient outcomes and survival. In this review, we <i>1</i>) highlight our current understanding of the microbial changes that occur with cachexia, <i>2</i>) discuss how microbial changes may contribute to adipose and skeletal muscle wasting, and <i>3</i>) outline study design considerations needed when examining the role of the microbiota in cancer-induced cachexia.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C661-C670"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11427007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141562429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Glucose influences endometrial receptivity to embryo implantation through O-GlcNAcylation-mediated regulation of the cytoskeleton. 葡萄糖通过 O-GlcNAcylation 介导的细胞骨架调节作用影响子宫内膜对胚胎植入的接受能力。
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-16 DOI: 10.1152/ajpcell.00559.2023
Peter T Ruane, Isabel Paterson, Beth Reeves, Daman Adlam, Stéphane C Berneau, Lewis Renshall, Jan J Brosens, Susan J Kimber, Daniel R Brison, John D Aplin, Melissa Westwood
{"title":"Glucose influences endometrial receptivity to embryo implantation through O-GlcNAcylation-mediated regulation of the cytoskeleton.","authors":"Peter T Ruane, Isabel Paterson, Beth Reeves, Daman Adlam, Stéphane C Berneau, Lewis Renshall, Jan J Brosens, Susan J Kimber, Daniel R Brison, John D Aplin, Melissa Westwood","doi":"10.1152/ajpcell.00559.2023","DOIUrl":"10.1152/ajpcell.00559.2023","url":null,"abstract":"<p><p>Phenotypic changes to endometrial epithelial cells underpin receptivity to embryo implantation at the onset of pregnancy but the effect of hyperglycemia on these processes remains poorly understood. Here, we show that physiological levels of glucose (5 mM) abolished receptivity in the endometrial epithelial cell line, Ishikawa. However, embryo attachment was supported by 17 mM glucose as a result of glucose flux through the hexosamine biosynthetic pathway (HBP) and modulation of cell function via protein O-GlcNAcylation. Pharmacological inhibition of HBP or protein O-GlcNAcylation reduced embryo attachment in cocultures at 17 mM glucose. Mass spectrometry analysis of the O-GlcNAcylated proteome in Ishikawa cells revealed that myosin phosphatase target subunit 1 (MYPT1) is more highly O-GlcNAcylated in 17 mM glucose, correlating with loss of its target protein, phospho-myosin light chain 2, from apical cell junctions of polarized epithelium. Two-dimensional (2-D) and three-dimensional (3-D) morphologic analysis demonstrated that the higher glucose level attenuates epithelial polarity through O-GlcNAcylation. Inhibition of Rho (ras homologous)A-associated kinase (ROCK) or myosin II led to reduced polarity and enhanced receptivity in cells cultured in 5 mM glucose, consistent with data showing that MYPT1 acts downstream of ROCK signaling. These data implicate regulation of endometrial epithelial polarity through RhoA signaling upstream of actomyosin contractility in the acquisition of endometrial receptivity. Glucose levels impinge on this pathway through O-GlcNAcylation of MYPT1, which may impact endometrial receptivity to an implanting embryo in women with diabetes.<b>NEW & NOTEWORTHY</b> Understanding how glucose regulates endometrial function will support preconception guidance and/or the development of targeted interventions for individuals living with diabetes wishing to embark on pregnancy. We found that glucose can influence endometrial epithelial cell receptivity to embryo implantation by regulating posttranslational modification of proteins involved in the maintenance of cell polarity. Impaired or inappropriate endometrial receptivity could contribute to fertility and/or early pregnancy complications caused by poor glucose control.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C634-C645"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Skeletal muscle hypertrophy: cell growth is cell growth. 回应反驳啮齿动物增效剂消融模型在确定骨骼肌肥大的分子和细胞机制方面的实用性。
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-29 DOI: 10.1152/ajpcell.00418.2024
Benjamin I Burke, Ahmed Ismaeel, Ferdinand von Walden, Kevin A Murach, John J McCarthy
{"title":"Skeletal muscle hypertrophy: cell growth is cell growth.","authors":"Benjamin I Burke, Ahmed Ismaeel, Ferdinand von Walden, Kevin A Murach, John J McCarthy","doi":"10.1152/ajpcell.00418.2024","DOIUrl":"10.1152/ajpcell.00418.2024","url":null,"abstract":"<p><p>Roberts et al. have provided an insightful counterpoint to our review article on the utility of the synergist ablation model. The purpose of this review is to provide some further dialogue regarding the strengths and weaknesses of the synergist ablation model. Specifically, we highlight that the robustness of the model overshadows surgical limitations. We also compare the transcriptomic responses to synergist ablation in mice and resistance exercise in humans to identify common pathways. We conclude that \"cell growth is cell growth\" and that the mechanisms available to cells to accumulate biomass and increase in size are similar across cell types and independent of the rate of growth.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C614-C618"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Alpha-ketoglutarate is required for chronic hypoxia-induced cardiac remodeling. 慢性缺氧诱导的心脏重塑需要α-酮戊二酸。
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-29 DOI: 10.1152/ajpcell.00257.2024
Daishi Tang, Yong Gu, Shasha Chen, Tong Niu, Jin'ao Zhu, Panpan Liu, Mingge Ding, Yanjie Guo
{"title":"Alpha-ketoglutarate is required for chronic hypoxia-induced cardiac remodeling.","authors":"Daishi Tang, Yong Gu, Shasha Chen, Tong Niu, Jin'ao Zhu, Panpan Liu, Mingge Ding, Yanjie Guo","doi":"10.1152/ajpcell.00257.2024","DOIUrl":"10.1152/ajpcell.00257.2024","url":null,"abstract":"<p><p>Chronic hypoxia (CH) is commonly associated with various cardiovascular diseases, with cardiac hypertrophy being the most frequently observed alteration. Metabolic remodeling is another consequence seen in the hypoxic heart. However, the mechanistic linkage between metabolic remodeling and cardiac hypertrophy in the hypoxic heart remains unclear. In this study, wild-type C57BL/6J mice were subjected to CH for 4 wk. Echocardiography and morphological analysis were used to assess the cardiac effects. We found that 4 wk of CH led to significant cardiac hypertrophy in the mice, whereas cardiac function remained unchanged compared with normoxic mice. In addition, CH induced an elevation in cardiac alpha-ketoglutarate (α-KG) content. Promoting α-KG degradation in the CH hearts prevented CH-induced cardiac hypertrophy but led to noticeable cardiac dysfunction. Mechanistically, α-KG promoted the transcription of hypertrophy-related genes by regulating histone methylation. Silencing lysine-specific demethylase 5 (KDM5), a histone demethylation enzyme, blunted α-KG-induced transcription of hypertrophy-related genes. These data suggest that α-KG is required for CH-induced cardiac remodeling, thus establishing a connection between metabolic changes and cardiac remodeling in hypoxic hearts.<b>NEW & NOTEWORTHY</b> We reported that alpha-ketoglutarate (α-KG) is indispensable for chronic hypoxia (CH)-induced cardiac remodeling, which builds the bridge between metabolic intermediates and cardiac remodeling.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C728-C736"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The risks and rewards of the synergist ablation model in skeletal muscle biology research. 协同消融模型在骨骼肌生物学研究中的风险与回报:编辑聚焦
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-29 DOI: 10.1152/ajpcell.00504.2024
Anika L Syroid, Thomas J Hawke
{"title":"The risks and rewards of the synergist ablation model in skeletal muscle biology research.","authors":"Anika L Syroid, Thomas J Hawke","doi":"10.1152/ajpcell.00504.2024","DOIUrl":"10.1152/ajpcell.00504.2024","url":null,"abstract":"","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C599-C600"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The utility of the rodent synergist ablation model in identifying molecular and cellular mechanisms of skeletal muscle hypertrophy. 啮齿动物增效剂消融模型在确定骨骼肌肥大的分子和细胞机制中的作用
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-29 DOI: 10.1152/ajpcell.00362.2024
Benjamin I Burke, Ahmed Ismaeel, John J McCarthy
{"title":"The utility of the rodent synergist ablation model in identifying molecular and cellular mechanisms of skeletal muscle hypertrophy.","authors":"Benjamin I Burke, Ahmed Ismaeel, John J McCarthy","doi":"10.1152/ajpcell.00362.2024","DOIUrl":"10.1152/ajpcell.00362.2024","url":null,"abstract":"<p><p>Skeletal muscle exhibits remarkable plasticity to adapt to stimuli such as mechanical loading. The mechanisms that regulate skeletal muscle hypertrophy due to mechanical overload have been thoroughly studied. Remarkably, our understanding of many of the molecular and cellular mechanisms that regulate hypertrophic growth were first identified using the rodent synergist ablation (SA) model and subsequently corroborated in human resistance exercise training studies. To demonstrate the utility of the SA model, we briefly summarize the hypertrophic mechanisms identified using the model and the following translation of these mechanism to human skeletal muscle hypertrophy induced by resistance exercise training.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C601-C606"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11427019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cell firing between ON alpha retinal ganglion cells and coupled amacrine cells in the mouse retina. 小鼠视网膜上α视网膜神经节细胞和耦合羊膜细胞之间的细胞发射。
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-07-16 DOI: 10.1152/ajpcell.00238.2024
Qin Wang, ChungHim So, Feng Pan
{"title":"Cell firing between ON alpha retinal ganglion cells and coupled amacrine cells in the mouse retina.","authors":"Qin Wang, ChungHim So, Feng Pan","doi":"10.1152/ajpcell.00238.2024","DOIUrl":"10.1152/ajpcell.00238.2024","url":null,"abstract":"<p><p>Gap junctions are channels that allow for direct transmission of electrical signals between cells. However, the ability of one cell to be impacted or controlled by other cells through gap junctions remains unclear. In this study, heterocellular coupling between ON α retinal ganglion cells (α-RGCs) and displaced amacrine cells (ACs) in the mouse retina was used as a model. The impact of the extent of coupling of interconnected ACs on the synchronized firing between coupled ON α-RGC-AC pair was investigated using the dopamine 1 receptor (D1R) antagonist-SCH23390 and agonist-SKF38393. It was observed that the synchronized firing between the ON α-RGC-ACs pairs was increased by the D1R antagonist SCH23390, whereas it was eradicated by the agonist SKF38393. Subsequently, the signaling drive was investigated by infecting coupled ON α-RGC-AC pairs with the channelrhodopsin-2(ChR2) mutation L132C engineered to enhance light sensitivities. The results demonstrated that the spikes of ON α-RGCs (without ChR2) could be triggered by ACs (with ChR2) through the gap junction, and vice versa. Furthermore, it was observed that ON α-RGCs stimulated with 3-10 Hz currents by whole cell patch could elicit synchronous spikes in the coupled ACs, and vice versa. This provided direct evidence that the firing of one cell could be influenced by another cell through gap junctions. However, this phenomenon was not observed between OFF α-RGC pairs. The study implied that the synchronized firing between ON α-RGC-AC pairs could potentially be affected by the coupling of interconnected ACs. Additionally, one cell type could selectively control the firing of another cell type, thereby forcefully transmitting information. The key role of gap junctions in synchronizing firing and driving cells between α-RGCs and coupled ACs in the mouse retina was highlighted.<b>NEW & NOTEWORTHY</b> This study investigates the role of gap junctions in transmitting electrical signals between cells and their potential for cell control. Using ON α retinal ganglion cells (α-RGCs) and amacrine cells (ACs) in the mouse retina, the researchers find that the extent of coupling between ACs affects synchronized firing. Bidirectional signaling occurs between ACs and ON α-RGCs through gap junctions.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C716-C727"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Muscular hyperplasia in Crohn's disease strictures: through thick and thin. 克罗恩病狭窄处的肌肉增生:厚积薄发。
IF 5 2区 生物学
American journal of physiology. Cell physiology Pub Date : 2024-09-01 Epub Date: 2024-06-24 DOI: 10.1152/ajpcell.00307.2024
Ido Veisman, William J Massey, Idan Goren, Weiwei Liu, Gaurav Chauhan, Florian Rieder
{"title":"Muscular hyperplasia in Crohn's disease strictures: through thick and thin.","authors":"Ido Veisman, William J Massey, Idan Goren, Weiwei Liu, Gaurav Chauhan, Florian Rieder","doi":"10.1152/ajpcell.00307.2024","DOIUrl":"10.1152/ajpcell.00307.2024","url":null,"abstract":"<p><p>Fibrostenosing Crohn's disease (CD) represents a challenging clinical condition characterized by the development of symptomatic strictures within the gastrointestinal tract. Despite therapeutic advancements in managing inflammation, the progression of fibrostenotic complications remains a significant concern, often necessitating surgical intervention. Recent investigations have unveiled the pivotal role of smooth muscle cell hyperplasia in driving luminal narrowing and clinical symptomatology. Drawing parallels to analogous inflammatory conditions affecting other organs, such as the airways and blood vessels, sheds light on common underlying mechanisms of muscular hyperplasia. This review synthesizes current evidence to elucidate the mechanisms underlying smooth muscle cell proliferation in CD-associated strictures, offering insights into potential therapeutic targets. By highlighting the emerging significance of muscle thickening as a novel therapeutic target, this review aims to inform future research endeavors and clinical strategies with the goal to mitigate the burden of fibrostenotic complications in CD and other conditions.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C671-C683"},"PeriodicalIF":5.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11427014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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