Due to ultrafine Nano-zinc particles are major component of PM0.1, so we aimed to investigate how ultrafine Nano-zinc particles effect on cardiac structure and function in myocardial infarction (MI) rabbits. We chose twenty-four New Zealand rabbits who were divided into sham group, MI group and MI exposure group randomly, 8 rabbits in each group. We preformed LAD ligation operation in MI group and MI exposure group. After two weeks rabbits suffered from MI successfully, we put the MI exposure group into ventilation chamber filled with 500ug/m3 ultrafine Nano-zinc particles for 6 hours per day. Sham group and MI group were raised in normal environment. Four weeks later, the heart function was detected using vevo2100 machine and all rabbits sacrificed, because we need to collect blood sample and heart tissue. According to echocardiography measurements, we found EF and FS both in MI group and MI exposure group decreased significantly, especially MI exposure group had severe decrease compared with MI group. In addition, left ventricular end-diastolic pressure (LVEDP) in MI exposure group increased obviously and LV +dp/dt max decreased significant. Both the formers in MI group changed to a lesser degree. HE staining results showed myocytes disorganization and LV wall thinning in MI and MI exposure groups. Masson trichrome staining showed that MI exposure group had maximum collagen. In summary, inhalation of ultrafine Nano-zinc particles indeed is harmful for MI rabbits. Moreover, ultrafine Nano-zinc particles can effect on myocardial systolic and diastolic function, thus promote the development from MI to heart failure.
{"title":"Effect of Ultrafine Nano-Zinc Particles on Cardiac Structure and Function in Myocardial Infarction Rabbits","authors":"Pei Niu, Li Li, Yufan Huang, Y. Huo","doi":"10.32604/MCB.2019.05724","DOIUrl":"https://doi.org/10.32604/MCB.2019.05724","url":null,"abstract":"Due to ultrafine Nano-zinc particles are major component of PM0.1, so we aimed to investigate how ultrafine Nano-zinc particles effect on cardiac structure and function in myocardial infarction (MI) rabbits. We chose twenty-four New Zealand rabbits who were divided into sham group, MI group and MI exposure group randomly, 8 rabbits in each group. We preformed LAD ligation operation in MI group and MI exposure group. After two weeks rabbits suffered from MI successfully, we put the MI exposure group into ventilation chamber filled with 500ug/m3 ultrafine Nano-zinc particles for 6 hours per day. Sham group and MI group were raised in normal environment. Four weeks later, the heart function was detected using vevo2100 machine and all rabbits sacrificed, because we need to collect blood sample and heart tissue. According to echocardiography measurements, we found EF and FS both in MI group and MI exposure group decreased significantly, especially MI exposure group had severe decrease compared with MI group. In addition, left ventricular end-diastolic pressure (LVEDP) in MI exposure group increased obviously and LV +dp/dt max decreased significant. Both the formers in MI group changed to a lesser degree. HE staining results showed myocytes disorganization and LV wall thinning in MI and MI exposure groups. Masson trichrome staining showed that MI exposure group had maximum collagen. In summary, inhalation of ultrafine Nano-zinc particles indeed is harmful for MI rabbits. Moreover, ultrafine Nano-zinc particles can effect on myocardial systolic and diastolic function, thus promote the development from MI to heart failure.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"99 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85279597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective：Thoracic endovascular aortic repair (TEVAR) of type B aortic dissection (AD) is to initiate the thrombosis in the false lumen to eventually result in aortic remodeling. We aim to find out whether the false lumen (FL) thrombosis rate after TEVAR can be predicted accurately by an index that expresses the degree of aortic arch angulation. Method: Three-dimensional aortic arch geometry of 39 type B AD patients (mean age: 48years) after TEVR were reconstructed from post-operative CT images. For the first time, the question mark which take into account the curvature of both aortic arch and the descending aorta was introduced to indicate the aortic arch morphology. The degree of question mark and the angles of aortic arch defined by previous literatures were measured. Moreover, hemodynamics for ADs with different question mark degree were numerically computed using different models. Result: No correlation between the aortic arch angles defined by previous researchers and the rate of thrombosis. However, the degree of question mark has negatively correlation with FL thrombosis (r=-.7394; p<.001). In addition, regions of recirculating flow and low wall shear stress (WSS) in the FLs decreased with the increase of the degree of question mark of the aorta. Conclusion: The degree of question mark proposed in this paper is a good description of the aortic arch geometry after TEVAR in patients with aortic B-type dissection. It is negatively correlated with postoperative FL thrombosis, the higher the question mark degree was, the less likely it was to form a complete thrombus.
{"title":"The Degree of Question Mark of Aorta Can Predict the Thrombosis Rate in the False Lumen of a Type-B Aortic Dissection After TEVAR","authors":"Da Li, Liqing Peng, Yi Wang, D. Yuan, T. Zheng","doi":"10.32604/MCB.2019.05718","DOIUrl":"https://doi.org/10.32604/MCB.2019.05718","url":null,"abstract":"Objective：Thoracic endovascular aortic repair (TEVAR) of type B aortic dissection (AD) is to initiate the thrombosis in the false lumen to eventually result in aortic remodeling. We aim to find out whether the false lumen (FL) thrombosis rate after TEVAR can be predicted accurately by an index that expresses the degree of aortic arch angulation. Method: Three-dimensional aortic arch geometry of 39 type B AD patients (mean age: 48years) after TEVR were reconstructed from post-operative CT images. For the first time, the question mark which take into account the curvature of both aortic arch and the descending aorta was introduced to indicate the aortic arch morphology. The degree of question mark and the angles of aortic arch defined by previous literatures were measured. Moreover, hemodynamics for ADs with different question mark degree were numerically computed using different models. Result: No correlation between the aortic arch angles defined by previous researchers and the rate of thrombosis. However, the degree of question mark has negatively correlation with FL thrombosis (r=-.7394; p<.001). In addition, regions of recirculating flow and low wall shear stress (WSS) in the FLs decreased with the increase of the degree of question mark of the aorta. Conclusion: The degree of question mark proposed in this paper is a good description of the aortic arch geometry after TEVAR in patients with aortic B-type dissection. It is negatively correlated with postoperative FL thrombosis, the higher the question mark degree was, the less likely it was to form a complete thrombus.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"138 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79817382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diabetes is a major risk factor to cause macrovascular diseases and plays a pivotal role in aortic wall remodeling. However, the effects of diabetes on elastic properties of aortas remain largely unknown. Thirty adult rabbits (1.6-2.2 kg) were collected and the type I diabetic rabbit model was induced by injection of alloxan. A total of 15 control and 15 diabetic rabbit (abdominal) aortas were harvested. Uniaxial and biaxial tensile tests were performed to measure ultimate tensile strength and to characterize biaxial mechanical behaviors of the aortas. A material model was fitted to the biaxial experimental data to obtain constitutive parameters. Histological and mass fraction analyses were performed to investigate the underlying microstructure and dry weight percentages of elastin and collagen in the control and the diabetic aortas. No statistically significant difference was found in ultimate tensile strength between the control and the diabetic aortas. Regarding biaxial mechanical responses, the diabetic aortas exhibited significantly lower extensibility and significantly higher tissue stiffness than the control aortas. Notably, tissue stiffening occurred in both circumferential and axial directions for the diabetic aortas; however, mechanical anisotropy does not change significantly. The material model was able to fit biaxial experimental data very well. Histology showed that a number of isolated foam cells were embedded in the diabetic aortas and hyperplasia of collagen was identified. The dry weight percentages of collagen within the diabetic aortas increased significantly as compared to the control aortas, whereas no significant change was found for that of elastin. The results suggest that the diabetes impairs elastic properties and alters microstructure of the aortas and consequently, these changes may further contribute to complex aortic wall remodeling.
{"title":"Mechanical Characterization and Constitutive Modeling of Rabbit Aortas in Health and Diabetes","authors":"Zhi Zhang, J. Tong","doi":"10.32604/MCB.2019.05721","DOIUrl":"https://doi.org/10.32604/MCB.2019.05721","url":null,"abstract":"Diabetes is a major risk factor to cause macrovascular diseases and plays a pivotal role in aortic wall remodeling. However, the effects of diabetes on elastic properties of aortas remain largely unknown. Thirty adult rabbits (1.6-2.2 kg) were collected and the type I diabetic rabbit model was induced by injection of alloxan. A total of 15 control and 15 diabetic rabbit (abdominal) aortas were harvested. Uniaxial and biaxial tensile tests were performed to measure ultimate tensile strength and to characterize biaxial mechanical behaviors of the aortas. A material model was fitted to the biaxial experimental data to obtain constitutive parameters. Histological and mass fraction analyses were performed to investigate the underlying microstructure and dry weight percentages of elastin and collagen in the control and the diabetic aortas. No statistically significant difference was found in ultimate tensile strength between the control and the diabetic aortas. Regarding biaxial mechanical responses, the diabetic aortas exhibited significantly lower extensibility and significantly higher tissue stiffness than the control aortas. Notably, tissue stiffening occurred in both circumferential and axial directions for the diabetic aortas; however, mechanical anisotropy does not change significantly. The material model was able to fit biaxial experimental data very well. Histology showed that a number of isolated foam cells were embedded in the diabetic aortas and hyperplasia of collagen was identified. The dry weight percentages of collagen within the diabetic aortas increased significantly as compared to the control aortas, whereas no significant change was found for that of elastin. The results suggest that the diabetes impairs elastic properties and alters microstructure of the aortas and consequently, these changes may further contribute to complex aortic wall remodeling.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79850413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oscillatory shear stress (OSS) is one of the major risk factors related to endothelial (EC) dysfunction, which contributes to atherosclerosis. Our previous study indicated that inhibitor of DNA binding1 (Id1) play vital role in the regulation of OSS mediated EC function related to atherosclerosis. However, the initiation mechanism during this process remains to be elucidated. Ten-eleven Translocation protein 1 alternative isoform (Tet1s) is a newly reported protein that may have function in adult tissue. Here, we investigate the role of Tet1s in regulating OSS mediated endothelial dysfunction and its underlying mechanism. First, physical interaction between Tet1s and Id1 was found and proved by immunoprecipitation. By using carotid partial ligation mice model in vivo and OSS applied on human umbilical venous endothelial cell (HUVEC) in vitro, we found that EC proliferation rate and adhesion molecule expression were upregulated in the local area with OSS characteristics. Compared to the grater curvature (laminar shear stress), a lower Tet1s expression level in atheroprone lesser curvature (OSS) suggested Tet1s regulate the EC function under OSS. This notion is supported by the decline of Tet1s expression in cell culture model. In order to explore the Tet1s expression regulated mechanism, the potential binding sites in Tet1s promoter region for CEBPB was identified by in silico analysis. By using PKA/CEBPB inhibitor H89, we found that H89 inhibited Tet1s expression. HUVEC cell proliferation, proinflammation gene expression as well as monocytes adhesion were enhanced after knockdown of Tet1s by specific siRNA. And overexpression of Tet1s eliminated OSS induced HUVEC proliferation and inflammation. Further studies revealed Tet1s negatively regulated the expression of Id1. Meanwhile, knockdown of Tet1s induced nucleocytoplasmic shuttling of Id1. Our finding indicates a significant role of Tet1s in regulating OSS mediated endothelial dysfunction with respect of abnormal proliferation and inflammation though Id1-dependent pathway.
{"title":"TET1 Alternative Isoform Regulates Oscillatory Shear Stress Induced Endothelial Dysfunction","authors":"Lu Huang, J. Qiu, Guixue Wang","doi":"10.32604/MCB.2019.05714","DOIUrl":"https://doi.org/10.32604/MCB.2019.05714","url":null,"abstract":"Oscillatory shear stress (OSS) is one of the major risk factors related to endothelial (EC) dysfunction, which contributes to atherosclerosis. Our previous study indicated that inhibitor of DNA binding1 (Id1) play vital role in the regulation of OSS mediated EC function related to atherosclerosis. However, the initiation mechanism during this process remains to be elucidated. Ten-eleven Translocation protein 1 alternative isoform (Tet1s) is a newly reported protein that may have function in adult tissue. Here, we investigate the role of Tet1s in regulating OSS mediated endothelial dysfunction and its underlying mechanism. \u0000 First, physical interaction between Tet1s and Id1 was found and proved by immunoprecipitation. By using carotid partial ligation mice model in vivo and OSS applied on human umbilical venous endothelial cell (HUVEC) in vitro, we found that EC proliferation rate and adhesion molecule expression were upregulated in the local area with OSS characteristics. Compared to the grater curvature (laminar shear stress), a lower Tet1s expression level in atheroprone lesser curvature (OSS) suggested Tet1s regulate the EC function under OSS. This notion is supported by the decline of Tet1s expression in cell culture model. In order to explore the Tet1s expression regulated mechanism, the potential binding sites in Tet1s promoter region for CEBPB was identified by in silico analysis. By using PKA/CEBPB inhibitor H89, we found that H89 inhibited Tet1s expression. HUVEC cell proliferation, proinflammation gene expression as well as monocytes adhesion were enhanced after knockdown of Tet1s by specific siRNA. And overexpression of Tet1s eliminated OSS induced HUVEC proliferation and inflammation. Further studies revealed Tet1s negatively regulated the expression of Id1. Meanwhile, knockdown of Tet1s induced nucleocytoplasmic shuttling of Id1. \u0000 Our finding indicates a significant role of Tet1s in regulating OSS mediated endothelial dysfunction with respect of abnormal proliferation and inflammation though Id1-dependent pathway.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"106 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88038656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qingyu Wang, D. Tang, G. Canton, Zheyang Wu, T. Hatsukami, K. Billiar, C. Yuan
Image-based computational models have been introduced to calculate plaque stress/strain conditions and investigate their association with plaque progression and rupture [Tang, Yang, Zheng, et al. (2004)]. However, the accuracy of the computational results is heavily dependent on the data and assumptions used by those models. Patient-specific vessel material properties are in general lacking in image-based computational models, limiting the accuracy of their stress/strain calculations. A noninvasive approach of combining in vivo 3D multi-contrast and Cine magnetic resonance imaging (MRI) and computational modeling was used to quantify patient-specific carotid plaque material properties for potential plaque model improvements [Wang, Canton, Guo, et al. (2017)]. The stress-based plaque vulnerability index (SPVI) was proposed to combine mechanical analysis, plaque morphology and composition for more complete carotid plaque vulnerability assessment.
基于图像的计算模型已经被引入计算斑块应力/应变条件，并研究它们与斑块进展和破裂的关系[Tang, Yang, Zheng, et .(2004)]。然而，计算结果的准确性在很大程度上取决于这些模型所使用的数据和假设。基于图像的计算模型通常缺乏患者特定的血管材料特性，从而限制了其应力/应变计算的准确性。采用一种无创的方法，结合体内三维多重对比和磁共振成像(MRI)以及计算建模，量化患者特定的颈动脉斑块材料特性，以潜在地改进斑块模型[Wang, Canton, Guo等(2017)]。提出基于应力的斑块易损性指数(SPVI)，将力学分析、斑块形态和组成相结合，更完整地评估颈动脉斑块易损性。
{"title":"Using 3D Thin-Layer Model with in Vivo Patient-Specific Vessel Material Properties to Assesse Carotid Atherosclerotic Plaque Vulnerability","authors":"Qingyu Wang, D. Tang, G. Canton, Zheyang Wu, T. Hatsukami, K. Billiar, C. Yuan","doi":"10.32604/MCB.2019.05748","DOIUrl":"https://doi.org/10.32604/MCB.2019.05748","url":null,"abstract":"Image-based computational models have been introduced to calculate plaque stress/strain conditions and investigate their association with plaque progression and rupture [Tang, Yang, Zheng, et al. (2004)]. However, the accuracy of the computational results is heavily dependent on the data and assumptions used by those models. Patient-specific vessel material properties are in general lacking in image-based computational models, limiting the accuracy of their stress/strain calculations. \u0000A noninvasive approach of combining in vivo 3D multi-contrast and Cine magnetic resonance imaging (MRI) and computational modeling was used to quantify patient-specific carotid plaque material properties for potential plaque model improvements [Wang, Canton, Guo, et al. (2017)]. The stress-based plaque vulnerability index (SPVI) was proposed to combine mechanical analysis, plaque morphology and composition for more complete carotid plaque vulnerability assessment.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"242 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80523629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The fluid mechanics community has been interested for many years in hemodynamics. More recently, significant endeavours of the solid mechanics community have permitted to establish constitutive equations and to achieve stress analyses in arterial lesions (atheromatous plaque in coronary or carotid arteries, aneurysms of the aorta). The mechanical properties of blood vessels have often been characterized ex vivo, but medical imaging, including MRI, now allows non-intrusive identifications in vivo. The spatial heterogeneity of these mechanical properties, even at the macroscopic scale, remains poorly explored despite its undeniable interest in understanding the mechanisms of remodeling and degeneration of the tissue. We are interested in the problem of identifying the fields of mechanical properties of aneurysms of the aorta. Scientific barriers are related to the complex geometry, the nonlinear and anisotropic behavior of tissues, the multiaxial loading conditions, and to the measurement of a local response in these tissues. Our identification approaches, based on digital image correlation field measurements and inverse methods, have demonstrated the link between the heterogeneity of mechanical properties and the existence of localized failure modes. A micromechanical approach has also made it possible to develop a mechanobiological model to reproduce the behavior of the aorta in surgical situations and a simulation software is being developed for assistance to personalized surgery in the cardiovascular field.
{"title":"Fluid Structure Interactions in Ascending Thoracic Aortic Aneurysms","authors":"S. Avril","doi":"10.32604/mcb.2019.05705","DOIUrl":"https://doi.org/10.32604/mcb.2019.05705","url":null,"abstract":"The fluid mechanics community has been interested for many years in hemodynamics. More recently, significant endeavours of the solid mechanics community have permitted to establish constitutive equations and to achieve stress analyses in arterial lesions (atheromatous plaque in coronary or carotid arteries, aneurysms of the aorta). The mechanical properties of blood vessels have often been characterized ex vivo, but medical imaging, including MRI, now allows non-intrusive identifications in vivo. The spatial heterogeneity of these mechanical properties, even at the macroscopic scale, remains poorly explored despite its undeniable interest in understanding the mechanisms of remodeling and degeneration of the tissue. We are interested in the problem of identifying the fields of mechanical properties of aneurysms of the aorta. Scientific barriers are related to the complex geometry, the nonlinear and anisotropic behavior of tissues, the multiaxial loading conditions, and to the measurement of a local response in these tissues. Our identification approaches, based on digital image correlation field measurements and inverse methods, have demonstrated the link between the heterogeneity of mechanical properties and the existence of localized failure modes. A micromechanical approach has also made it possible to develop a mechanobiological model to reproduce the behavior of the aorta in surgical situations and a simulation software is being developed for assistance to personalized surgery in the cardiovascular field.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86789427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kun Peng, Xinyang Cui, A. Qiao, M. Ohta, K. Shimoyama, Y. Mu
Biodegradable stents which can avoid risks caused by incompatibility between artery and permanent stents are attracting much interests. However, biodegradable stents have not been extensively applied in clinical therapy because of their insufficient scaffold performance as a result of poor Young’s Modulus of biodegradable materials and weaken structures in degradation process. In this study, a patented stent and a common stent were simulated to degrade in a 40% stenotic vesel based on a corrosion model involving uniform corrosion and stress corrosion. In the degradation process, the scaffold performance of the two stents and their functionality on reshaping diseased vessels are analyzed. The results showed that radial recoiling ratio and mass loss ratio of the common stent is 22.6% and 14.1%, respectively. In comparison, radial recoiling ratio and mass loss ratio of the common stent are definitely lower than those of the common stent, at the value of 7.19% and 3.1%. It is indicated that the patented stent still has a stronger scaffold performance compared with the common stent. Besides, with positive influence of the patented stent on stenotic vessel, a larger and flatter lumen was observed in the plaque deployed with the patented stent. It implies that mechanical performance of biodegradable stents and their functionality highly depend on their geometries. Owing to improved mechanical performance induced by structural innovation, the novel biodegradable zinc alloy stent is promised to be an alternative choice in intervention surgeries.
{"title":"Mechanical Analysis of a Novel Biodegradable Zinc Alloy Stent Based on Degradation Model","authors":"Kun Peng, Xinyang Cui, A. Qiao, M. Ohta, K. Shimoyama, Y. Mu","doi":"10.32604/mcb.2019.05729","DOIUrl":"https://doi.org/10.32604/mcb.2019.05729","url":null,"abstract":"Biodegradable stents which can avoid risks caused by incompatibility between artery and permanent stents are attracting much interests. However, biodegradable stents have not been extensively applied in clinical therapy because of their insufficient scaffold performance as a result of poor Young’s Modulus of biodegradable materials and weaken structures in degradation process. In this study, a patented stent and a common stent were simulated to degrade in a 40% stenotic vesel based on a corrosion model involving uniform corrosion and stress corrosion. In the degradation process, the scaffold performance of the two stents and their functionality on reshaping diseased vessels are analyzed. The results showed that radial recoiling ratio and mass loss ratio of the common stent is 22.6% and 14.1%, respectively. In comparison, radial recoiling ratio and mass loss ratio of the common stent are definitely lower than those of the common stent, at the value of 7.19% and 3.1%. It is indicated that the patented stent still has a stronger scaffold performance compared with the common stent. Besides, with positive influence of the patented stent on stenotic vessel, a larger and flatter lumen was observed in the plaque deployed with the patented stent. It implies that mechanical performance of biodegradable stents and their functionality highly depend on their geometries. Owing to improved mechanical performance induced by structural innovation, the novel biodegradable zinc alloy stent is promised to be an alternative choice in intervention surgeries.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"67 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89986114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this article, we summarize our previous work in imaging-based computational modelling and simulation of the interaction between blood flow and atherosclerotic plaque. We also discussed our recent developments in multiphysical modelling of plaque progression and destabilization. Significance and translation of the modelling study to clinical practice are discussed in order to better assess plaque vulnerability and accurately predict a possible rupture.
{"title":"Atherosclerotic Plaque Rupture Prediction: Imaging-Based Computational Simulation and Multiphysical Modelling","authors":"Zhiyong Li","doi":"10.32604/mcb.2019.06308","DOIUrl":"https://doi.org/10.32604/mcb.2019.06308","url":null,"abstract":"In this article, we summarize our previous work in imaging-based computational modelling and simulation of the interaction between blood flow and atherosclerotic plaque. We also discussed our recent developments in multiphysical modelling of plaque progression and destabilization. Significance and translation of the modelling study to clinical practice are discussed in order to better assess plaque vulnerability and accurately predict a possible rupture.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"2029 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91319109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In order to improve the calculation accuracy of computed tomography angiography-derived fractional flow reserve (FFRCT), a mathematical model for setting the patient-specific flow boundary condition was proposed, in which some independent physiological parameters, such as myocardial mass, diastolic blood pressure, heart rate and vessel volume were considered. This model was employed to simulate hemodynamics in sixteen patients with coronary stenosis. The results of FFRCT demonstrated good consistency with invasively measured FFR. The diagnostic accuracy of FFRCT was 85%. The proposed model offers a new approach to improve the accuracy of FFRCT, as well as promotes the clinical application of FFRCT.
{"title":"Approach to the Flow Rate Distribution of Coronary Branches in the Calculation of Fractional Flow Reserve","authors":"A. Qiao, Honghui Zhang, Jun Xia","doi":"10.32604/MCB.2019.05715","DOIUrl":"https://doi.org/10.32604/MCB.2019.05715","url":null,"abstract":"In order to improve the calculation accuracy of computed tomography angiography-derived fractional flow reserve (FFRCT), a mathematical model for setting the patient-specific flow boundary condition was proposed, in which some independent physiological parameters, such as myocardial mass, diastolic blood pressure, heart rate and vessel volume were considered. This model was employed to simulate hemodynamics in sixteen patients with coronary stenosis. The results of FFRCT demonstrated good consistency with invasively measured FFR. The diagnostic accuracy of FFRCT was 85%. The proposed model offers a new approach to improve the accuracy of FFRCT, as well as promotes the clinical application of FFRCT.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90272344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiumei Guan, Hong Li, Xin Li, Xiaoyun Zhang, Xiaodong Cui, Hong Yan, YuzhenWang, Shunmei Liu, Min Cheng
Endothelial progenitor cells (EPCs) play an important role in postnatal angiogenesis and neovascularization. Previous studies have revealed shear stress could accelerate EPC proliferation, differentiation, migration and so on, which contribute to postnatal angiogenesis and neovascularization. Moreover, some studies indicate that autophagy actively participates angiogenesis by affecting EPC migration and differentiation. Here, we try to elucidate the possible roles of autophagy of EPC differentiation induced by shear stress. Methods and Results：EPCs were exposed to shear stress (12 dyne/cm2). And then the expression of autophagy markers, such as LC3Ⅱ/Ⅰ,P62andATG5, were analyzed using Western blot. The results have shown that in EPCs, shear stress triggered an increase in LC3Ⅱ/Ⅰ and ATG5 at 10 min, which was then followed by a decrease. In contrast, shear stress caused a decrease in P62 at 10 min, which was then followed by an increase. Furthermore, immunostaining revealed that the unsheared cells showed only weak LCⅡ staining. However, shear stress increased LCⅡ staining. Bafromycin experiment confirmed that the increase of autophagy caused by shear stress was due to an increase in the formation of autophagy rather than a decrease in the degradation of autophagosomes. To examine the role of autophagy in the shear stress-induced EPC differentiation, we pretreated late EPCs with 3-MA, an inhibitor of autophagy, before the application of shear stress. Through real time RT-PCR and FACS analyses, we observed that the pretreatment of EPCs with 3-MA significantly inhibited the shear stress induced up-regulation of vWF and CD31. In the mean time, treatment of EPCs with LY294002 (a small molecule inhibitor of PI3K) or KLF2 siRNA inhibited the shear stress-induced EPC autophagy and differentiation. Conclusion：Autophagy is involved in the shear stress-upregulated expression of endothelial markers vWF and CD31 in EPCs. Moreover, this increase was observed to be mediated by PI3K and KLF2. Although further studies are needed to confirm the relationship between these mechanosensitive molecules, the present results may provide new insights into the relationship between EPC autophagy and differentiation induced by shear stress.
{"title":"The Role of Autophagy in the Differentiation of EPCs Induced by Shear Stress","authors":"Xiumei Guan, Hong Li, Xin Li, Xiaoyun Zhang, Xiaodong Cui, Hong Yan, YuzhenWang, Shunmei Liu, Min Cheng","doi":"10.32604/MCB.2019.05755","DOIUrl":"https://doi.org/10.32604/MCB.2019.05755","url":null,"abstract":"Endothelial progenitor cells (EPCs) play an important role in postnatal angiogenesis and neovascularization. Previous studies have revealed shear stress could accelerate EPC proliferation, differentiation, migration and so on, which contribute to postnatal angiogenesis and neovascularization. Moreover, some studies indicate that autophagy actively participates angiogenesis by affecting EPC migration and differentiation. Here, we try to elucidate the possible roles of autophagy of EPC differentiation induced by shear stress. Methods and Results：EPCs were exposed to shear stress (12 dyne/cm2). And then the expression of autophagy markers, such as LC3Ⅱ/Ⅰ,P62andATG5, were analyzed using Western blot. The results have shown that in EPCs, shear stress triggered an increase in LC3Ⅱ/Ⅰ and ATG5 at 10 min, which was then followed by a decrease. In contrast, shear stress caused a decrease in P62 at 10 min, which was then followed by an increase. Furthermore, immunostaining revealed that the unsheared cells showed only weak LCⅡ staining. However, shear stress increased LCⅡ staining. Bafromycin experiment confirmed that the increase of autophagy caused by shear stress was due to an increase in the formation of autophagy rather than a decrease in the degradation of autophagosomes. To examine the role of autophagy in the shear stress-induced EPC differentiation, we pretreated late EPCs with 3-MA, an inhibitor of autophagy, before the application of shear stress. Through real time RT-PCR and FACS analyses, we observed that the pretreatment of EPCs with 3-MA significantly inhibited the shear stress induced up-regulation of vWF and CD31. In the mean time, treatment of EPCs with LY294002 (a small molecule inhibitor of PI3K) or KLF2 siRNA inhibited the shear stress-induced EPC autophagy and differentiation. Conclusion：Autophagy is involved in the shear stress-upregulated expression of endothelial markers vWF and CD31 in EPCs. Moreover, this increase was observed to be mediated by PI3K and KLF2. Although further studies are needed to confirm the relationship between these mechanosensitive molecules, the present results may provide new insights into the relationship between EPC autophagy and differentiation induced by shear stress.","PeriodicalId":48719,"journal":{"name":"Molecular & Cellular Biomechanics","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82189195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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