The aim of this study was to investigate the anatomical features of the mitral isthmus (MI) line, the vessels located there and their localisation in the MI line.
Methods
MI length and wall thickness were measured in a total of 65 autopsied fresh hearts. The distances of the vessels at the level of MI to the left inferior pulmonary vein (LIPV), mitral annulus (MA), endocardium surface (ES) and lateral adipose tissue (LAT) were recorded.
Results
The mean linear length of MI and left atrial wall thickness were 49.6 ± 9.9 mm and 3.9 ± 1.2 mm, respectively. GCV and LCx are approximately 1 cm from MA, 4 cm from LIPV, 5-6 mm from ES and 7 mm from LAT. Great cardiac vein (GCV) was found to be located in the MI line in 100 %, left circumflex artery (LCx) in 60 %, and vein of Marshall (VOM) in 63.1 % of cases. Presence of only GCV was recorded as Type-1 (18.5 %), GCV and LCx as Type-2 (18.5 %), GCV and VOM as Type-3 (21.5 %) and presence of all three as Type-4 (41.5 %). LCx located below the GCV was recorded as Type-A (59 %), above the GCV as Type-B (25.6 %), and at the same level but with LCx on the endocardial surface as Type-C1 (12.8 %) and on the epicardial surface as Type-C2 (2.6 %).
Conclusion
This study proves that the anatomy of MI is far from standardised and helps to raise awareness of the vascular pattern that may be encountered prior to ablation intervention.
{"title":"Mitral Isthmus anatomy: Detailed examination and classification proposal","authors":"Buse Naz Çandır Gürses , Kader Yılar , Çağla Ergin , Özcan Gayretli","doi":"10.1016/j.carpath.2025.107723","DOIUrl":"10.1016/j.carpath.2025.107723","url":null,"abstract":"<div><h3>Aim</h3><div>The aim of this study was to investigate the anatomical features of the mitral isthmus (MI) line, the vessels located there and their localisation in the MI line.</div></div><div><h3>Methods</h3><div>MI length and wall thickness were measured in a total of 65 autopsied fresh hearts. The distances of the vessels at the level of MI to the left inferior pulmonary vein (LIPV), mitral annulus (MA), endocardium surface (ES) and lateral adipose tissue (LAT) were recorded.</div></div><div><h3>Results</h3><div>The mean linear length of MI and left atrial wall thickness were 49.6 ± 9.9 mm and 3.9 ± 1.2 mm, respectively. GCV and LCx are approximately 1 cm from MA, 4 cm from LIPV, 5-6 mm from ES and 7 mm from LAT. Great cardiac vein (GCV) was found to be located in the MI line in 100 %, left circumflex artery (LCx) in 60 %, and vein of Marshall (VOM) in 63.1 % of cases. Presence of only GCV was recorded as Type-1 (18.5 %), GCV and LCx as Type-2 (18.5 %), GCV and VOM as Type-3 (21.5 %) and presence of all three as Type-4 (41.5 %). LCx located below the GCV was recorded as Type-A (59 %), above the GCV as Type-B (25.6 %), and at the same level but with LCx on the endocardial surface as Type-C1 (12.8 %) and on the epicardial surface as Type-C2 (2.6 %).</div></div><div><h3>Conclusion</h3><div>This study proves that the anatomy of MI is far from standardised and helps to raise awareness of the vascular pattern that may be encountered prior to ablation intervention.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"76 ","pages":"Article 107723"},"PeriodicalIF":2.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Foramen ovale plays a key role in foetal circulation, however it may remain patent after birth throughout the life. Its patency is so frequent in healthy people (27-35 %), such as to be considered a variant of normal. It is at risk of complications, like paradoxical embolism by right to left shunt with stroke, migraine, temporary blindness, as well as aneurysm, thrombosis and endocarditis of the fossa ovalis. There is no doubt that it should be considered a congenital heart disease at all effects. Invasive cardiology closure with umbrella and even with stiches is nowadays feasible and indicated in specific clinical scenarios. Further research is needed to determine whether cardiac echo-doppler screening for identifing affected patients as a primary prevention measure is advisable.
{"title":"Patent foramen ovale: A variant of normal or a true congenital heart disease?","authors":"Stefania Rizzo, Monica De Gaspari, Cristina Basso, Chiara Fraccaro, Gaetano Thiene","doi":"10.1016/j.carpath.2025.107722","DOIUrl":"10.1016/j.carpath.2025.107722","url":null,"abstract":"<div><div>Foramen ovale plays a key role in foetal circulation, however it may remain patent after birth throughout the life. Its patency is so frequent in healthy people (27-35 %), such as to be considered a variant of normal. It is at risk of complications, like paradoxical embolism by right to left shunt with stroke, migraine, temporary blindness, as well as aneurysm, thrombosis and endocarditis of the fossa ovalis. There is no doubt that it should be considered a congenital heart disease at all effects. Invasive cardiology closure with umbrella and even with stiches is nowadays feasible and indicated in specific clinical scenarios. Further research is needed to determine whether cardiac echo-doppler screening for identifing affected patients as a primary prevention measure is advisable.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"76 ","pages":"Article 107722"},"PeriodicalIF":2.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-02-17DOI: 10.1016/j.carpath.2025.107726
L. Maximilian Buja , Michelle M. McDonald , Bihong Zhao , Navneet Narula , Jagat Narula , Rolf F. Barth
Context
Ischemic heart disease (IHD) due to coronary atherosclerosis constitutes the leading cause of morbidity and mortality worldwide. This review was undertaken to document the historical basis for our contemporary understanding of atherosclerosis-based disease and to provide a rationale for continued support for autopsy-based research to make further progress in reducing the morbidity and mortality from atherosclerosis-related disease.
Objectives
To analyze the contributions of the autopsy-initiated pathological studies to complement and validate other lines of investigation in determining the pathology and pathogenesis of the leading worldwide cause of morbidity and mortality, namely, atherosclerosis and its major complications of coronary atherosclerosis, ischemic heart disease, coronary thrombosis, acute myocardial infarction, and sudden cardiac death.
Data sources
Systematic search on PubMed to gather relevant studies concerning autopsy studies and reviews of the pathology and pathogenesis of atherosclerosis, ischemic heart disease, coronary atherosclerosis, coronary thrombosis, myocardial infarction, and sudden cardiac death
Conclusions
Extensive published reports have confirmed the continuing importance of the autopsy as a powerful tool to understand the pathogenesis, clinical features, and therapeutic options for major diseases. This specifically has been shown by the analysis of atherosclerosis and its major manifestation of ischemic heart disease, as presented in this (Part I) and its companion (Part II) review. Autopsy-initiated pathological studies have documented the prevalence and natural history of atherosclerosis in different human populations in relationship to the prevalence of risk factors and established that the clinically silent phase of the disease begins in the first decades of life. Insights from these studies have been essential in developing and evaluating strategies for continued progress in preventing and controlling the disability and death associated with atherosclerotic heart disease.
{"title":"Insights from autopsy-initiated pathological studies of the pathogenesis and clinical manifestations of atherosclerosis and ischemic heart disease: Part I. Atherosclerosis","authors":"L. Maximilian Buja , Michelle M. McDonald , Bihong Zhao , Navneet Narula , Jagat Narula , Rolf F. Barth","doi":"10.1016/j.carpath.2025.107726","DOIUrl":"10.1016/j.carpath.2025.107726","url":null,"abstract":"<div><h3>Context</h3><div>Ischemic heart disease (IHD) due to coronary atherosclerosis constitutes the leading cause of morbidity and mortality worldwide. This review was undertaken to document the historical basis for our contemporary understanding of atherosclerosis-based disease and to provide a rationale for continued support for autopsy-based research to make further progress in reducing the morbidity and mortality from atherosclerosis-related disease.</div></div><div><h3>Objectives</h3><div>To analyze the contributions of the autopsy-initiated pathological studies to complement and validate other lines of investigation in determining the pathology and pathogenesis of the leading worldwide cause of morbidity and mortality, namely, atherosclerosis and its major complications of coronary atherosclerosis, ischemic heart disease, coronary thrombosis, acute myocardial infarction, and sudden cardiac death.</div></div><div><h3>Data sources</h3><div>Systematic search on PubMed to gather relevant studies concerning autopsy studies and reviews of the pathology and pathogenesis of atherosclerosis, ischemic heart disease, coronary atherosclerosis, coronary thrombosis, myocardial infarction, and sudden cardiac death</div></div><div><h3>Conclusions</h3><div>Extensive published reports have confirmed the continuing importance of the autopsy as a powerful tool to understand the pathogenesis, clinical features, and therapeutic options for major diseases. This specifically has been shown by the analysis of atherosclerosis and its major manifestation of ischemic heart disease, as presented in this (Part I) and its companion (Part II) review. Autopsy-initiated pathological studies have documented the prevalence and natural history of atherosclerosis in different human populations in relationship to the prevalence of risk factors and established that the clinically silent phase of the disease begins in the first decades of life. Insights from these studies have been essential in developing and evaluating strategies for continued progress in preventing and controlling the disability and death associated with atherosclerotic heart disease.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"76 ","pages":"Article 107726"},"PeriodicalIF":2.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2024-12-27DOI: 10.1016/j.carpath.2024.107711
Ashmeetha Manilall , Lebogang Mokotedi , Sulè Gunter , Regina Le Roux , Serena Fourie , Aletta ME Millen
Background
Interleukin-6 (IL-6) is an attractive therapeutic target due to its diverse roles in the pathogenesis of conditions characterized by systemic inflammation. IL-6 has also been implicated in the pathophysiology of heart failure. This study aimed to investigate the impact of IL-6 receptor blockade with tocilizumab on the molecular pathways underlying systemic inflammation-induced left ventricular (LV) dysfunction in a collagen-induced arthritis (CIA) rat model.
Methods
Seventy-three Sprague-Dawley rats were divided into three groups: control (n=28), CIA (n=29), and CIA+IL-6 blocker (n=16). Inflammation was induced in the CIA and CIA+IL-6 blocker groups using bovine type II collagen emulsified in incomplete Freund's adjuvant. After arthritis onset, the CIA+IL-6 blocker group received tocilizumab for six weeks. Circulating inflammatory markers, relative LV mRNA gene expressions, and LV systolic and diastolic function were assessed.
Results
CIA rats developed LV diastolic and early-stage LV systolic dysfunction, which was not ameliorated by IL-6 blocker administration (p > 0.05). IL-6 blocker administration did not impact circulating inflammatory markers (all p > 0.05) or LV mRNA expression of inflammatory markers compared to the CIA group, nor did it reverse inflammation-induced increases in LV mRNA expression of genes involved in fibrosis and collagen turnover, regulation of titin phosphorylation, Ca2+ handling, mitochondrial function, or apoptosis (all p > 0.05). However, LV mRNA expressions of CD68 and LOX, genes involved in macrophage infiltration and collagen cross-linking, were increased in the CIA group (p = 0.03, p = 0.0004), but not in the CIA+IL-6 blocker group compared to controls (p > 0.05).
Conclusion
These results suggest that although IL-6 blockade by tocilizumab may prevent inflammation-induced collagen cross-linking, the current treatment regimen may not protect against inflammation-induced LV dysfunction. Therefore, the role of IL-6 in the molecular mechanisms of inflammation-induced LV dysfunction remains inconclusive.
{"title":"Tocilizumab does not ameliorate inflammation-induced left ventricular dysfunction in a collagen-induced arthritis rat model","authors":"Ashmeetha Manilall , Lebogang Mokotedi , Sulè Gunter , Regina Le Roux , Serena Fourie , Aletta ME Millen","doi":"10.1016/j.carpath.2024.107711","DOIUrl":"10.1016/j.carpath.2024.107711","url":null,"abstract":"<div><h3>Background</h3><div>Interleukin-6 (IL-6) is an attractive therapeutic target due to its diverse roles in the pathogenesis of conditions characterized by systemic inflammation. IL-6 has also been implicated in the pathophysiology of heart failure. This study aimed to investigate the impact of IL-6 receptor blockade with tocilizumab on the molecular pathways underlying systemic inflammation-induced left ventricular (LV) dysfunction in a collagen-induced arthritis (CIA) rat model.</div></div><div><h3>Methods</h3><div>Seventy-three Sprague-Dawley rats were divided into three groups: control (n=28), CIA (n=29), and CIA+IL-6 blocker (n=16). Inflammation was induced in the CIA and CIA+IL-6 blocker groups using bovine type II collagen emulsified in incomplete Freund's adjuvant. After arthritis onset, the CIA+IL-6 blocker group received tocilizumab for six weeks. Circulating inflammatory markers, relative LV mRNA gene expressions, and LV systolic and diastolic function were assessed.</div></div><div><h3>Results</h3><div>CIA rats developed LV diastolic and early-stage LV systolic dysfunction, which was not ameliorated by IL-6 blocker administration (<em>p</em> > 0.05). IL-6 blocker administration did not impact circulating inflammatory markers (all <em>p</em> > 0.05) or LV mRNA expression of inflammatory markers compared to the CIA group, nor did it reverse inflammation-induced increases in LV mRNA expression of genes involved in fibrosis and collagen turnover, regulation of titin phosphorylation, Ca<sup>2+</sup> handling, mitochondrial function, or apoptosis (all <em>p</em> > 0.05). However, LV mRNA expressions of <em>CD68</em> and <em>LOX</em>, genes involved in macrophage infiltration and collagen cross-linking, were increased in the CIA group (<em>p</em> = 0.03, <em>p</em> = 0.0004), but not in the CIA+IL-6 blocker group compared to controls (<em>p</em> > 0.05).</div></div><div><h3>Conclusion</h3><div>These results suggest that although IL-6 blockade by tocilizumab may prevent inflammation-induced collagen cross-linking, the current treatment regimen may not protect against inflammation-induced LV dysfunction. Therefore, the role of IL-6 in the molecular mechanisms of inflammation-induced LV dysfunction remains inconclusive.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107711"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2024-12-31DOI: 10.1016/j.carpath.2024.107712
Armin Darius Peivandi , Michael Holtkamp , Hennes Rave , Lars Linsen , Sven Martens , Klaus-Michael Müller , Uwe Karst , Sabrina Martens
Objectives
Re-operations due to material degeneration carry a burden for patients with congenital heart disease (CHD). The study aim was to compare rapid vs. slow degeneration of biomaterials in CHD patients.
Methods
Explants from re-operations of 29 CHD patients (2015-2022) were grouped according to the duration of implantation (short implantation < 3 years (n = 16) vs. long implantation 10-15 years (n = 13)). Histologic processing and staining allowed tissue and calcification analysis. Micro-X-ray fluorescence (µXRF) was used for elemental analysis. Semi-quantitative comparison of calcium was conducted using a self-developed software.
Results
Thrombosis was recurrently observed in short-implanted RVOT samples. 62.5 % (n = 10) of short-implanted samples showed calcification in Alizarin red staining, in comparison to 69.2 % (n = 9) in the long-implanted group. µXRF analysis revealed calcium deposits in all patients, mostly co-localized with phosphorus. In the short implant group, other detected elements included iron, chlorine, chromium, nickel, titanium and zinc. In the long implant group, iron, nickel, titanium, zinc, copper and iodine were found. No significant difference in calcification (Ca-Si-ratio) between both implantation groups (p = 0.083) was found.
Conclusion
Thrombus formation is a main rapid degeneration cause in the RVOT. Deteriorations of biomaterials in CHD patients show strong parallels to bioprosthetic valve degenerations. Early calcification in young patients is supported by our semi-quantitative calcium analysis. The role of other elements in graft degeneration remains to be assessed in the future.
{"title":"Rapid versus slow degeneration and complications of biomaterials in patients with congenital heart disease","authors":"Armin Darius Peivandi , Michael Holtkamp , Hennes Rave , Lars Linsen , Sven Martens , Klaus-Michael Müller , Uwe Karst , Sabrina Martens","doi":"10.1016/j.carpath.2024.107712","DOIUrl":"10.1016/j.carpath.2024.107712","url":null,"abstract":"<div><h3>Objectives</h3><div>Re-operations due to material degeneration carry a burden for patients with congenital heart disease (CHD). The study aim was to compare rapid vs. slow degeneration of biomaterials in CHD patients.</div></div><div><h3>Methods</h3><div>Explants from re-operations of 29 CHD patients (2015-2022) were grouped according to the duration of implantation (short implantation < 3 years (n = 16) vs. long implantation 10-15 years (n = 13)). Histologic processing and staining allowed tissue and calcification analysis. Micro-X-ray fluorescence (µXRF) was used for elemental analysis. Semi-quantitative comparison of calcium was conducted using a self-developed software.</div></div><div><h3>Results</h3><div>Thrombosis was recurrently observed in short-implanted RVOT samples. 62.5 % (n = 10) of short-implanted samples showed calcification in Alizarin red staining, in comparison to 69.2 % (n = 9) in the long-implanted group. µXRF analysis revealed calcium deposits in all patients, mostly co-localized with phosphorus. In the short implant group, other detected elements included iron, chlorine, chromium, nickel, titanium and zinc. In the long implant group, iron, nickel, titanium, zinc, copper and iodine were found. No significant difference in calcification (Ca-Si-ratio) between both implantation groups (p = 0.083) was found.</div></div><div><h3>Conclusion</h3><div>Thrombus formation is a main rapid degeneration cause in the RVOT. Deteriorations of biomaterials in CHD patients show strong parallels to bioprosthetic valve degenerations. Early calcification in young patients is supported by our semi-quantitative calcium analysis. The role of other elements in graft degeneration remains to be assessed in the future.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107712"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-01-06DOI: 10.1016/j.carpath.2025.107716
Alice Nassar , Elizabeth Wagura , Marios Loukas
Vascular occlusive diseases remain a major health burden worldwide, necessitating a deeper understanding of the adaptive responses that mitigate their impact. Arteriogenesis, the growth and remodeling of collateral vessels in response to arterial occlusion, is a vital defense mechanism that counteracts fluid shear stress-induced vascular stenosis or occlusion. While physical factors driving arteriogenesis have been extensively studied, the specific cellular mediators involved are poorly understood. Notably, the role of innate and adaptive immune cells, particularly mast cells, in arteriogenesis has received limited attention. This systematic review bridges this knowledge gap by investigating the contribution of mast cells to vascular cell proliferation and leukocyte recruitment in arteriogenesis. A comprehensive search of major databases using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines reveals the critical connection between mast cells, inflammatory cells, innate immune cells, and growth factors in arteriogenesis. Our findings highlight the molecular mechanisms of mast cell activation, sheer stress exertion, and pro-arteriogenic growth factor recruitment. Furthermore, we explore the endogenous and exogenous factors, including nitrite, dipyridamole, thrombin, and cobra venom, triggering mast cell-mediated release of pro-arteriogenic factors. Additionally, we examine the impact of recombinant parathyroid hormone (rPTH) therapy on mast cell numbers and arteriogenesis in bone defect and allograft healing. Our review provides compelling evidence for the pro-arteriogenic role of mast cells, particularly during the early inflammatory phase of vessel occlusion, suggesting that targeting mast cell activation may be a promising therapeutic strategy for enhancing arteriogenesis and treating ischemia-related diseases.
{"title":"Mast cells and arteriogenesis: A systematic review","authors":"Alice Nassar , Elizabeth Wagura , Marios Loukas","doi":"10.1016/j.carpath.2025.107716","DOIUrl":"10.1016/j.carpath.2025.107716","url":null,"abstract":"<div><div>Vascular occlusive diseases remain a major health burden worldwide, necessitating a deeper understanding of the adaptive responses that mitigate their impact. Arteriogenesis, the growth and remodeling of collateral vessels in response to arterial occlusion, is a vital defense mechanism that counteracts fluid shear stress-induced vascular stenosis or occlusion. While physical factors driving arteriogenesis have been extensively studied, the specific cellular mediators involved are poorly understood. Notably, the role of innate and adaptive immune cells, particularly mast cells, in arteriogenesis has received limited attention. This systematic review bridges this knowledge gap by investigating the contribution of mast cells to vascular cell proliferation and leukocyte recruitment in arteriogenesis. A comprehensive search of major databases using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines reveals the critical connection between mast cells, inflammatory cells, innate immune cells, and growth factors in arteriogenesis. Our findings highlight the molecular mechanisms of mast cell activation, sheer stress exertion, and pro-arteriogenic growth factor recruitment. Furthermore, we explore the endogenous and exogenous factors, including nitrite, dipyridamole, thrombin, and cobra venom, triggering mast cell-mediated release of pro-arteriogenic factors. Additionally, we examine the impact of recombinant parathyroid hormone (rPTH) therapy on mast cell numbers and arteriogenesis in bone defect and allograft healing. Our review provides compelling evidence for the pro-arteriogenic role of mast cells, particularly during the early inflammatory phase of vessel occlusion, suggesting that targeting mast cell activation may be a promising therapeutic strategy for enhancing arteriogenesis and treating ischemia-related diseases.</div></div>","PeriodicalId":9451,"journal":{"name":"Cardiovascular Pathology","volume":"75 ","pages":"Article 107716"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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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