Pub Date : 2025-12-19DOI: 10.1016/j.jacbts.2025.101449
Saffie Mohran PhD , Kristina B. Kooiker PhD , Ateeqa Naim BS , Matvey Pilagov BS , Anthony Asencio BS , Kyrah L. Turner BS , Weikang Ma PhD , Galina Flint MD. , Siyao Jiang BS , Jing Zhao BS , Timothy S. McMillen PhD , Christian Mandrycky PhD , Max Mahoney-Schaefer BS , Thomas C. Irving PhD , Bertrand C.W. Tanner PhD , Neil M. Kad PhD , Michael Regnier PhD , Farid Moussavi-Harami MD
We investigated the effects of aficamten on cardiac muscle structure, biochemical activity, and contractile function. Aficamten does not structurally sequester myosin heads along the thick filament. It inhibits ATPase activity by decreasing myosin ATPase cycling kinetics, with the emergence of a super slow biochemical nucleotide turnover. This results in decreased force and calcium sensitivity without altering cross-bridge cycling. Our myofibril mechanical assay showed inhibition of force with accelerated relaxation. In engineered heart tissues, while mavacamten and aficamten inhibit cardiac twitch forces, mavacamten reduces the activation kinetics while both accelerate relaxation.
{"title":"Myosin Modulator Aficamten Inhibits Force by Altering Myosin’s Biochemical Activity Without Changing Thick Filament Structure","authors":"Saffie Mohran PhD , Kristina B. Kooiker PhD , Ateeqa Naim BS , Matvey Pilagov BS , Anthony Asencio BS , Kyrah L. Turner BS , Weikang Ma PhD , Galina Flint MD. , Siyao Jiang BS , Jing Zhao BS , Timothy S. McMillen PhD , Christian Mandrycky PhD , Max Mahoney-Schaefer BS , Thomas C. Irving PhD , Bertrand C.W. Tanner PhD , Neil M. Kad PhD , Michael Regnier PhD , Farid Moussavi-Harami MD","doi":"10.1016/j.jacbts.2025.101449","DOIUrl":"10.1016/j.jacbts.2025.101449","url":null,"abstract":"<div><div>We investigated the effects of aficamten on cardiac muscle structure, biochemical activity, and contractile function. Aficamten does not structurally sequester myosin heads along the thick filament. It inhibits ATPase activity by decreasing myosin ATPase cycling kinetics, with the emergence of a super slow biochemical nucleotide turnover. This results in decreased force and calcium sensitivity without altering cross-bridge cycling. Our myofibril mechanical assay showed inhibition of force with accelerated relaxation. In engineered heart tissues, while mavacamten and aficamten inhibit cardiac twitch forces, mavacamten reduces the activation kinetics while both accelerate relaxation.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 1","pages":"Article 101449"},"PeriodicalIF":8.4,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145789023","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 : 2025-12-19DOI: 10.1016/j.jacbts.2025.101435
Rana Hamouche MD , Sean M. Tatum PhD , Elizabeth Dranow PhD , J. Alan Maschek PhD , Christos P. Kyriakopoulos MD , Thirupura S. Shankar PhD , Joseph R. Visker PhD , Jing Ling AS , Konstantinos Sideris MD , Craig H. Selzman MD , Abdallah G. Kfoury MD , Josef Stehlik MD, MPH , Rami Alharethi MD , James C. Fang MD , TingTing Hong MD, PhD , Sutip Navankasattusas PhD , Matthew T. Rondina MD , William L. Holland PhD , Scott A. Summers PhD , Stavros G. Drakos MD, PhD , Eleni Tseliou MD, PhD
Myocardial recovery after left ventricular assist device (LVAD) support is a critical phenomenon that allows advanced heart failure patients to retain their native heart. We quantified targeted sphingolipids in serum and cardiac tissue of patients who exhibited recovery post-LVAD. Our analysis revealed sustained elevated circulating ceramides levels in nonresponders post-LVAD, whereas responders showed reduced sphingosine-1-phosphate (S1P) levels. In contrast, cardiac tissue from nonresponders displayed increased S1P levels. We suggest that diminished ceramide and S1P may contribute to an increased likelihood of recovery after LVAD support. Collectively, our findings implicate the sphingolipid metabolic pathway as a potential therapeutic target to promote myocardial recovery after mechanical support.
{"title":"The Role of Sphingolipids in Myocardial Recovery Mediated by Mechanical Unloading and Circulatory Support","authors":"Rana Hamouche MD , Sean M. Tatum PhD , Elizabeth Dranow PhD , J. Alan Maschek PhD , Christos P. Kyriakopoulos MD , Thirupura S. Shankar PhD , Joseph R. Visker PhD , Jing Ling AS , Konstantinos Sideris MD , Craig H. Selzman MD , Abdallah G. Kfoury MD , Josef Stehlik MD, MPH , Rami Alharethi MD , James C. Fang MD , TingTing Hong MD, PhD , Sutip Navankasattusas PhD , Matthew T. Rondina MD , William L. Holland PhD , Scott A. Summers PhD , Stavros G. Drakos MD, PhD , Eleni Tseliou MD, PhD","doi":"10.1016/j.jacbts.2025.101435","DOIUrl":"10.1016/j.jacbts.2025.101435","url":null,"abstract":"<div><div>Myocardial recovery after left ventricular assist device (LVAD) support is a critical phenomenon that allows advanced heart failure patients to retain their native heart. We quantified targeted sphingolipids in serum and cardiac tissue of patients who exhibited recovery post-LVAD. Our analysis revealed sustained elevated circulating ceramides levels in nonresponders post-LVAD, whereas responders showed reduced sphingosine-1-phosphate (S1P) levels. In contrast, cardiac tissue from nonresponders displayed increased S1P levels. We suggest that diminished ceramide and S1P may contribute to an increased likelihood of recovery after LVAD support. Collectively, our findings implicate the sphingolipid metabolic pathway as a potential therapeutic target to promote myocardial recovery after mechanical support.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 1","pages":"Article 101435"},"PeriodicalIF":8.4,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145788487","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 : 2025-12-15DOI: 10.1016/j.jacbts.2025.101433
Libo Wang PhD , Xulei Duan MS , Huibing Liu PhD , Fei Lin PhD , Chaoyuan Zhou MD , Katrin Schröder PhD , Ajay M. Shah MD , Guoan Zhao MD, PhD , Min Zhang MD, PhD
Previous studies have shown that Nox4 activates eIF2α/ATF4 signaling during the integrated stress response (ISR) and protects heart injury. However, their roles in calcific aortic valve disease (CAVD) remain unclear. Here, we show that both ATF4 and Nox4 are up-regulated in porcine aortic valve interstitial cells (AVIC) and in human aortic valves with CAVD. Nox4 knockdown promotes while Nox4 overexpression suppresses CAVD by modulating ISR. Importantly, ISR activators Guanabenz and Sephin1 effectively attenuate AVIC osteoblastic-like differentiation and mitigate CAVD in rabbits and mice, respectively. These findings highlight that pharmacological enhancement of the ISR is a promising therapeutic strategy for CAVD.
{"title":"Pharmacological Enhancement of Integrated Stress Response Confers Protection in Calcific Aortic Valve Disease","authors":"Libo Wang PhD , Xulei Duan MS , Huibing Liu PhD , Fei Lin PhD , Chaoyuan Zhou MD , Katrin Schröder PhD , Ajay M. Shah MD , Guoan Zhao MD, PhD , Min Zhang MD, PhD","doi":"10.1016/j.jacbts.2025.101433","DOIUrl":"10.1016/j.jacbts.2025.101433","url":null,"abstract":"<div><div>Previous studies have shown that Nox4 activates eIF2α/ATF4 signaling during the integrated stress response (ISR) and protects heart injury. However, their roles in calcific aortic valve disease (CAVD) remain unclear. Here, we show that both ATF4 and Nox4 are up-regulated in porcine aortic valve interstitial cells (AVIC) and in human aortic valves with CAVD. Nox4 knockdown promotes while Nox4 overexpression suppresses CAVD by modulating ISR. Importantly, ISR activators Guanabenz and Sephin1 effectively attenuate AVIC osteoblastic-like differentiation and mitigate CAVD in rabbits and mice, respectively. These findings highlight that pharmacological enhancement of the ISR is a promising therapeutic strategy for CAVD.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 1","pages":"Article 101433"},"PeriodicalIF":8.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768124","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 : 2025-12-11DOI: 10.1016/j.jacbts.2025.101434
Bob S.L. Lee PhD , Joshua K. Dunn BSc , Cassandra Liang BSc , Grace Chensee BSc , Renhua Song PhD , Cassandra Malecki PhD , Elizabeth N. Robertson MD, PhD , Gavin J. Sutton PhD , Christopher P. Stanley PhD , Brett D. Hambly MD, PhD , Xiangjian Zheng PhD , Paul G. Bannon MD, PhD , Wai Ho Tang PhD , Justin J.-L. Wong PhD , Renjing Liu PhD
Vascular calcification arises from the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) and is a hallmark of many cardiovascular pathologies. This study identifies Tet2, a DNA demethylase, as a critical epigenetic regulator that prevents this phenotypic switch. VSMC-specific loss of Tet2 promotes osteogenic differentiation, apoptosis, increased infiltration of Trem2hi macrophages and medial aortic calcification. High-dose ascorbate used to enhance Tet2 activity significantly reduced calcification and preserved aortic structure in mice. These findings support Tet2 reactivation as a potential therapeutic strategy to prevent or reverse vascular calcification in cardiovascular disease.
{"title":"Epigenetic Reprogramming via TET2 Prevents Medial Calcification and Restores Vascular Smooth Muscle Cell Identity","authors":"Bob S.L. Lee PhD , Joshua K. Dunn BSc , Cassandra Liang BSc , Grace Chensee BSc , Renhua Song PhD , Cassandra Malecki PhD , Elizabeth N. Robertson MD, PhD , Gavin J. Sutton PhD , Christopher P. Stanley PhD , Brett D. Hambly MD, PhD , Xiangjian Zheng PhD , Paul G. Bannon MD, PhD , Wai Ho Tang PhD , Justin J.-L. Wong PhD , Renjing Liu PhD","doi":"10.1016/j.jacbts.2025.101434","DOIUrl":"10.1016/j.jacbts.2025.101434","url":null,"abstract":"<div><div>Vascular calcification arises from the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) and is a hallmark of many cardiovascular pathologies. This study identifies Tet2, a DNA demethylase, as a critical epigenetic regulator that prevents this phenotypic switch. VSMC-specific loss of Tet2 promotes osteogenic differentiation, apoptosis, increased infiltration of Trem2<sup>hi</sup> macrophages and medial aortic calcification. High-dose ascorbate used to enhance Tet2 activity significantly reduced calcification and preserved aortic structure in mice. These findings support Tet2 reactivation as a potential therapeutic strategy to prevent or reverse vascular calcification in cardiovascular disease.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 1","pages":"Article 101434"},"PeriodicalIF":8.4,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145718952","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 : 2025-11-17DOI: 10.1016/j.jacbts.2025.101409
Maximilian Y. Emmert MD, PhD , Johannes Holzmeister MD , Ole Blank MSc , Heike Meyborg MSc , Anne Jomard PhD , Giulia Mearini PhD , Maria Vono PhD , Miriam Weisskopf DVM, PhD , Marco Michalski PhD , Chandan Kadur Nagaraju PhD , Mark Dehdashtian BSc , Dominic Hollamby MA , Chris Rusconi PhD , Steven Zelenkofske MD , Volkmar Falk MD , Eduard Ayuso DVM, PhD , Josef El Andari PhD , Nikola Cesarovic DVM, PhD
Safe and efficient in vivo delivery of advanced therapies (ATs) remains a major challenge hindering their path to clinical adoption. We present a novel, fully percutaneous, catheter-based locoregional perfusion (LRP) system for targeted delivery of ATs, minimizing systemic exposure. Using principles from extracorporeal membrane oxygenation and cardiovascular perfusion, we developed and validated the LRP concept in porcine models, focusing on the kidney as a clinically relevant target. Custom catheter prototypes enabled safe, isolated perfusion of the kidney. Using adeno-associated viruses (AAVs) as model cargos, LRP achieved up to 69,000-fold higher vector retention within the LRP circulation than systemic circulation, and significantly reduced delivery to off-target organs such as the liver and spleen. AAV5 showed the highest transduction efficiency, with up to 75-fold greater gene expression. These findings demonstrate the feasibility, safety, and precision of LRP for organ-specific AT delivery while preventing plausible off-target toxicity. It may therefore represent a unique platform for next-generation delivery of AT and potentially beyond, including other therapeutic agents such as pharmaco- or chemotherapy to the target-organ.
{"title":"Next-Generation Percutaneous Catheter–Based Closed-Loop Perfusion Concept Enables High-Precision Organ Delivery of Advanced Therapies","authors":"Maximilian Y. Emmert MD, PhD , Johannes Holzmeister MD , Ole Blank MSc , Heike Meyborg MSc , Anne Jomard PhD , Giulia Mearini PhD , Maria Vono PhD , Miriam Weisskopf DVM, PhD , Marco Michalski PhD , Chandan Kadur Nagaraju PhD , Mark Dehdashtian BSc , Dominic Hollamby MA , Chris Rusconi PhD , Steven Zelenkofske MD , Volkmar Falk MD , Eduard Ayuso DVM, PhD , Josef El Andari PhD , Nikola Cesarovic DVM, PhD","doi":"10.1016/j.jacbts.2025.101409","DOIUrl":"10.1016/j.jacbts.2025.101409","url":null,"abstract":"<div><div>Safe and efficient in vivo delivery of advanced therapies (ATs) remains a major challenge hindering their path to clinical adoption. We present a novel, fully percutaneous, catheter-based locoregional perfusion (LRP) system for targeted delivery of ATs, minimizing systemic exposure. Using principles from extracorporeal membrane oxygenation and cardiovascular perfusion, we developed and validated the LRP concept in porcine models, focusing on the kidney as a clinically relevant target. Custom catheter prototypes enabled safe, isolated perfusion of the kidney. Using adeno-associated viruses (AAVs) as model cargos, LRP achieved up to 69,000-fold higher vector retention within the LRP circulation than systemic circulation, and significantly reduced delivery to off-target organs such as the liver and spleen. AAV5 showed the highest transduction efficiency, with up to 75-fold greater gene expression. These findings demonstrate the feasibility, safety, and precision of LRP for organ-specific AT delivery while preventing plausible off-target toxicity. It may therefore represent a unique platform for next-generation delivery of AT and potentially beyond, including other therapeutic agents such as pharmaco- or chemotherapy to the target-organ.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 12","pages":"Article 101409"},"PeriodicalIF":8.4,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145549536","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 : 2025-11-15DOI: 10.1016/j.jacbts.2025.101395
Matthew A. Muller MS , Elliot Luttrell-Williams MS , Hannah Bash BS , Macintosh G. Cornwell PhD , H. Michael Belmont MD , Peter Izmirly MD , Haley Rosmann BS , Michael S. Garshick MD , Tessa J. Barrett PhD , Stuart Katz MD , Kelly V. Ruggles PhD , Jill P. Buyon MD , Jeffrey S. Berger MD, MS
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with an increased risk of vascular dysfunction and cardiovascular disease. We validate our previously developed Systemic Lupus Erythematosus Activity Platelet-Gene Expression Signature (SLAP-GES) score and investigate its relationship with platelet activity and vascular health. SLAP-GES was associated with the SLE Disease Activity Index (Padj < 0.001) and consistent over time (r = 0.76; P = 9 × 10−5). Moreover, SLAP-GES was associated increased platelet aggregation in response to submaximal epinephrine (P = 0.084), leukocyte platelet aggregates (P = 0.014), and neutrophil platelet aggregates (P = 0.043). SLAP-GES was also associated with impaired glycocalyx (P = 0.011) and brachial artery flow-mediated dilation (P = 0.045). Altogether, SLAP-GES is associated with SLE disease activity, platelet activity, and impaired vascular health.
{"title":"Platelet Gene Expression in Systemic Lupus Erythematosus and Cardiovascular Health","authors":"Matthew A. Muller MS , Elliot Luttrell-Williams MS , Hannah Bash BS , Macintosh G. Cornwell PhD , H. Michael Belmont MD , Peter Izmirly MD , Haley Rosmann BS , Michael S. Garshick MD , Tessa J. Barrett PhD , Stuart Katz MD , Kelly V. Ruggles PhD , Jill P. Buyon MD , Jeffrey S. Berger MD, MS","doi":"10.1016/j.jacbts.2025.101395","DOIUrl":"10.1016/j.jacbts.2025.101395","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is a complex autoimmune disease with an increased risk of vascular dysfunction and cardiovascular disease. We validate our previously developed Systemic Lupus Erythematosus Activity Platelet-Gene Expression Signature (SLAP-GES) score and investigate its relationship with platelet activity and vascular health. SLAP-GES was associated with the SLE Disease Activity Index (<em>Padj</em> < 0.001) and consistent over time (r = 0.76; <em>P =</em> 9 × 10<sup>−5</sup>). Moreover, SLAP-GES was associated increased platelet aggregation in response to submaximal epinephrine <em>(P =</em> 0.084), leukocyte platelet aggregates <em>(P =</em> 0.014), and neutrophil platelet aggregates <em>(P =</em> 0.043). SLAP-GES was also associated with impaired glycocalyx <em>(P =</em> 0.011) and brachial artery flow-mediated dilation <em>(P =</em> 0.045). Altogether, SLAP-GES is associated with SLE disease activity, platelet activity, and impaired vascular health.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 12","pages":"Article 101395"},"PeriodicalIF":8.4,"publicationDate":"2025-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519324","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 : 2025-11-12DOI: 10.1016/j.jacbts.2025.101411
Wahid Abu-Amer MD , Khaled Shorbaji MBBS , Rodrigo Meade BA , Sophia R. Pyeatte MD , Larisa Belaygorod MD , Mohamed S. Zaghloul MD , Shahab Hafezi MBBS , Louai Alrata MBBS , Amanda Penrose BA , Batool Arif MS , Stephen G. Wu PhD , Clay F. Semenkovich MD , Mohamed A. Zayed MD, PhD, MBA
There are currently no reliable serum biomarkers to aid in the diagnosis of peripheral artery disease (PAD). We hypothesized that circulating fatty acid synthase (cFAS) can be an independent diagnostic biomarker for PAD. Serum cFAS and demographics were compared for patients with and without PAD or chronic limb threatening ischemia (CLTI). Patients with PAD or CLTI had significantly higher serum cFAS content. We observed optimal cutoffs for cFAS in distinguishing between individuals with and without PAD or CLTI. Our study demonstrates that cFAS is an independent serum-based diagnostic biomarker for PAD, can distinguish between patients with PAD vs CLTI, and may predict disease severity.
{"title":"Serum cFAS Content Correlates With Incidence of Peripheral Arterial Disease","authors":"Wahid Abu-Amer MD , Khaled Shorbaji MBBS , Rodrigo Meade BA , Sophia R. Pyeatte MD , Larisa Belaygorod MD , Mohamed S. Zaghloul MD , Shahab Hafezi MBBS , Louai Alrata MBBS , Amanda Penrose BA , Batool Arif MS , Stephen G. Wu PhD , Clay F. Semenkovich MD , Mohamed A. Zayed MD, PhD, MBA","doi":"10.1016/j.jacbts.2025.101411","DOIUrl":"10.1016/j.jacbts.2025.101411","url":null,"abstract":"<div><div>There are currently no reliable serum biomarkers to aid in the diagnosis of peripheral artery disease (PAD). We hypothesized that circulating fatty acid synthase (cFAS) can be an independent diagnostic biomarker for PAD. Serum cFAS and demographics were compared for patients with and without PAD or chronic limb threatening ischemia (CLTI). Patients with PAD or CLTI had significantly higher serum cFAS content. We observed optimal cutoffs for cFAS in distinguishing between individuals with and without PAD or CLTI. Our study demonstrates that cFAS is an independent serum-based diagnostic biomarker for PAD, can distinguish between patients with PAD vs CLTI, and may predict disease severity.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 12","pages":"Article 101411"},"PeriodicalIF":8.4,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145493113","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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