Biomechanics and Modeling in Mechanobiology最新文献

{"title":"Should perilymph be considered when modeling the lateral semicircular canal?","authors":"Manon Blaise,&nbsp;Daniel Baumgartner,&nbsp;Anne Charpiot","doi":"10.1007/s10237-026-02086-2","DOIUrl":"10.1007/s10237-026-02086-2","url":null,"abstract":"<div><p>The inner ear contains a set of sensors that detect head accelerations, and are responsible for our proper balance. Due to its small size and fragility, numerical models are an essential tool to compensate for the lack of direct biomechanical experiments on the inner ear’s tissues. In existing models, the surrounding perilymphatic compartment is seldom represented, imposing rigid boundary conditions on the endolymphatic compartment. Using an original 2.5D finite element model of the lateral semicircular canal, we demonstrate that both perilymph dynamics and membranous labyrinth elasticity significantly influence cupula biomechanical behavior (cupula displacement amplitude and von Mises stress distribution). Based on the cupula’s time constant, we also propose new viscoelastic law parameters to best describe its behavior. A numerical simulation of a reference clinical test, in which canal rotation was abruptly stopped within 100 ms, was implemented as a stimulus to the models. In the complete model incorporating the perilymph compartment, the cupula exhibited, as expected, a rapid deflection toward the canal followed by a slow return to its straight position. Conversely, in the absence of the perilymphatic compartment, the cupula demonstrated oscillatory-like behavior, deflecting initially slightly toward the canal and then toward the utricle before returning to its straight position. The implications of accounting for the anatomical (i.e., flexible) boundary conditions of the membranous labyrinth are discussed, highlighting their importance for accurately capturing vestibular mechanics and for improving the understanding of related pathophysiological conditions.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baseline state for pulmonary vasculature with pulmonary arterial hypertension: effect of geometric remodeling and metabolic shift","authors":"Haritha N. Mullagura,&nbsp;Hamidreza Gharahi,&nbsp;C. Alberto Figueroa,&nbsp;Seungik Baek","doi":"10.1007/s10237-026-02076-4","DOIUrl":"10.1007/s10237-026-02076-4","url":null,"abstract":"<div><p>Pulmonary arterial hypertension (PAH) is a complex disease characterized by chronically elevated pulmonary arterial pressure, with early onset and progression linked to structural, metabolic, and morphological changes in the pulmonary vasculature. Understanding the interplay between hemodynamics and arterial wall mechanics is essential to capture the pathology of the distal vasculature in PAH. This study aims to develop a data-driven framework that establishes a baseline state of PAH vasculature, incorporating key features of arterial wall constituents, geometry, and their interaction with PAH-specific hemodynamics. Illustrative examples of symmetrically bifurcating arterial trees are used to define representative baseline characteristics of PAH-affected pulmonary arteries. Compared with healthy homeostatic vasculature, the computational results demonstrate pronounced geometric and mechanical alterations: Arterial stiffness increases from approximately 7–10 kPa in healthy arteries to 300–800 kPa in PAH, representing a ~ 40–85 times increase across generations. Because wall thickening is imposed from histological measurements while outer diameter is preserved, the diameter-to-thickness ratio (D/h) decreases from ~ 14 in healthy arteries to ~ 3.8 in PAH, reflecting severe lumen narrowing and medial hypertrophy. In addition, the metabolic energy cost per unit length in PAH is more than double that of healthy arteries when assuming unchanged metabolic consumption per unit volume, whereas enforcing equal total energy cost yields a reduced per-volume metabolic consumption of ~ 450–500 W/m³. These findings suggest that maintaining constant metabolic consumption per unit volume would impose excessive energetic demand on the pulmonary vasculature in PAH, whereas redistribution of metabolic expenditure through altered wall composition may represent a more physiologically plausible adaptation. Furthermore, this framework provides a quantitative baseline state for PAH vasculature and lays the groundwork for future integration of growth-and-remodeling analyses and pharmacological pathway modeling to evaluate treatment response.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02076-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Towards personalization of 1D blood flow models: sensitivity analysis and parameter calibration","authors":"L. A. Mansilla Alvarez,&nbsp;D. de Oliveira Mussolin,&nbsp;G. Cunha-Lima,&nbsp;S. Garzon,&nbsp;L. O. Müller,&nbsp;P. A. Lemos,&nbsp;P. J. Blanco","doi":"10.1007/s10237-026-02094-2","DOIUrl":"10.1007/s10237-026-02094-2","url":null,"abstract":"<div><p>In this work, we address one of the central challenges in translational computational hemodynamics: how to effectively individualize cardiovascular models in scenarios where patient data are scarce and the parameter space is large. We propose an approach to construct patient-specific 1D blood flow models from patient data; specifically, the methodology relies on calibrating model parameters using a limited set of flow rate and pressure measurements. As a model to describe the systemic circulation, we adopt a simplified version of the Anatomically Detailed Arterial Network model which is combined with a Covariance Matrix Adaptation Evolutionary Strategy (CMA-ES) to find the best set of parameters that minimize the discrepancy metric between model prediction and available measurements. The calibration problem is addressed in two steps. In the first one, the influence of each physical parameter on the personalization process is quantified via an exhaustive global sensitivity analysis. Then, CMA-ES is employed to estimate the optimal model parameters. The findings of this study demonstrate the feasibility of deriving accurate patient-specific models in a setting characterized by small data and a high-dimensional parameter space. Furthermore, we provide a comprehensive analysis of the regional impact of physical parameters on the waveform characterization and their potential impact on clinically relevant biomarkers.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02094-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of catheter navigation through flexible intracranial vessel: a combined in silico and in vitro study","authors":"Mahesh S. Nagargoje,&nbsp;Demitria A. Poulos,&nbsp;Virginia Fregona,&nbsp;Giulia Luraghi,&nbsp;Francesco Migliavacca,&nbsp;Bryan C. Good,&nbsp;Jose Felix Rodriguez Matas","doi":"10.1007/s10237-026-02089-z","DOIUrl":"10.1007/s10237-026-02089-z","url":null,"abstract":"<div><p>Trackability of thrombectomy catheters through tortuous cerebral vessels is a key determinant of mechanical thrombectomy success, particularly for large-bore aspiration catheters. Yet, the underlying biomechanical challenges remain unclear. This study integrates in silico and in vitro analyses to investigate catheter navigation in a flexible intracranial vasculature model. A silicone patient-averaged tortuous vessel model was used for experimental studies in a circulatory flow loop and reconstructed from CT imaging for computational simulations. Regarding the in silico part of the study, in contrast to prior work relying on tip-dragging or centerline-based advancement, we implemented clinically realistic catheter pushing mechanics. We varied the vessel compliance and catheter–vessel friction coefficients to understand their sensitivity toward navigation. Strong qualitative agreement emerged between simulated and experimental catheter paths. Key findings include: (i) realistic pushing produced trajectories distinct from tip-dragging, with the catheter naturally aligning along the outer curvature to generate supportive contact and it matches with in vitro experiments; (ii) increased vessel flexibility (2 MPa) markedly improved catheter advancement, whereas stiffer vessels (10 MPa and rigid) promoted kinking; (iii) catheter–vessel interaction was observed to be a critical factor in navigation, with low friction coefficient (F) enhancing trackability (F &lt; 0.1) and high friction (F &gt; 0.15) triggering bending and kinking. Incorporating vessel flexibility and clinically representative pushing mechanics is essential for accurate thrombectomy modeling. The presented framework accurately reproduces catheter behavior, particularly in curved segments, and offers predictive capabilities for device performance. These insights offer quantitative design guidance for next-generation microcatheters and aspiration catheters, highlighting the critical role of catheter–vessel mechanics in distal cerebral arteries.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148172687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simple non-invasive in vivo measurement of stress difference in the skin","authors":"Hannah Conroy Broderick,&nbsp;Wenting Shu,&nbsp;Aisling Ní Annaidh,&nbsp;Michel Destrade","doi":"10.1007/s10237-026-02087-1","DOIUrl":"10.1007/s10237-026-02087-1","url":null,"abstract":"<div><p>Accurate, non-invasive quantification of in vivo skin stress would improve surgical planning and objective assessment of skin mechanics. We present a simple acousto-elastic approach that estimates the in vivo in-plane stress difference from surface wave speeds measured along two orthogonal directions on the skin. For a large class of incompressible hyperelastic anisotropic models with one family of parallel fibres aligned with the skin tension lines, we show that the principal Cauchy stress difference satisfies: <span>(sigma _1 - sigma _2 simeq rho (v_text {max}^2 - v_text {min}^2))</span>, where <span>(rho )</span> is the tissue mass density, and <span>(v_text {max})</span>, <span>(v_text {min})</span> are the Rayleigh wave speeds along, and orthogonal to, the direction of greatest tension, respectively, with a relative error below 9 percent. We validate the formula with finite element simulations in plane strain using the neo-Hookean and Holzapfel-Gasser-Ogden materials. In the neo-Hookean case, stress differences calculated from simulated wave speeds agree with the ground truth within 2.3 to 7.9 percent across pre-stretches <span>(lambda _1 = 1.05)</span> to 1.20. In the anisotropic case with fibres parallel to the principal pre-stress, the error is 0.25 to 2.81 percent over the same range. These results provide a proof of concept for estimating the in-plane stress difference in skin from orthogonal Rayleigh-wave speeds, within the assumptions of a homogeneous fibre-reinforced hyperelastic model.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02087-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A biphasic modeling framework for arterial compressibility under steady axisymmetric deformation","authors":"Takeo Fujiwara,&nbsp;Shukei Sugita,&nbsp;Shigeo Wada,&nbsp;Tomohiro Otani","doi":"10.1007/s10237-026-02082-6","DOIUrl":"10.1007/s10237-026-02082-6","url":null,"abstract":"<div><p>Arterial walls contain large amounts of water and have conventionally been modeled as incompressible. However, recent experimental studies have reported non-negligible arterial compressibility, with volumetric changes on the order of 10% or larger depending on loading conditions. To clarify the mechanical origin and its implications, this study develops a biphasic modeling framework for arterial mechanics, in which apparent compressibility arises from interstitial fluid transfer within the arterial wall. The arterial wall is modeled as a saturated biphasic material consisting of a solid skeleton and interstitial fluid, in which the solid skeleton is modeled as an anisotropic, hyperelastic material with macroscopic volumetric deformability, and the fluid motion is governed by Darcy’s law. Assuming steady, axisymmetric plane-strain deformation, the resulting nonlinear mechanical equilibrium is reduced to a one-dimensional radial boundary-value problem and solved numerically using a finite element method. Systematic parametric analyses demonstrate that radial and circumferential deformations, as well as the resulting volumetric changes, are consistent with experimentally observed mean values, with deviations within 2% under the same loading conditions. Such volumetric expansion, driven by the hydrostatic pressure of the interstitial fluid, induces tensile stress components in the radial direction within the solid skeleton, revealing a mechanical consequence of fluid–solid interactions that is not directly accessible from apparent deformation measures alone. These findings suggest that biphasic modeling provides a mechanically interpretable framework for examining arterial wall responses in regimes where fluid–solid interactions are relevant.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02082-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal modeling of tau aggregation following traumatic brain injury: implications for chronic traumatic encephalopathy","authors":"José González-Cabrero,&nbsp;Carlos G. S. Cardoso,&nbsp;Inés Moreno-González,&nbsp;Ricardo J. Alves-de-Sousa","doi":"10.1007/s10237-026-02092-4","DOIUrl":"10.1007/s10237-026-02092-4","url":null,"abstract":"<div><p>Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder associated with repetitive traumatic brain injury (TBI) and characterized by abnormal tau aggregation. Although biological and clinical evidence link head trauma to tau pathology, the mechanistic pathway connecting mechanical impact to biochemical progression remains insufficiently defined. This research introduces a mathematical model designed to predict the spatiotemporal evolution of tau accumulation following TBI. The formulation is based on an Avrami-type nucleation–growth framework, originally developed for phase transformations in materials, here adapted to represent the initiation and expansion of tau aggregates. Nucleation rate and growth velocity are treated as time-dependent parameters to capture realistic pathological dynamics. Temporal kinetics are calibrated using experimental data from mouse models of tauopathy, ensuring agreement with observed global progression. Spatial heterogeneity is incorporated through a mechanical field derived from finite element simulations, enabling regions exposed to higher post-impact strain to exhibit faster local transformation. This integrated biomechanical–mathematical approach provides a quantitative link between injury-induced deformation and tau aggregation, offering a basis for identifying mechanically vulnerable regions that may be predisposed to CTE-related pathology.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02092-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A monolithic patient-specific 3D–0D model for In silico investigation of hemodynamics in patients with left ventricular assist devices","authors":"Mia Bonini,&nbsp;Marc Hirschvogel,&nbsp;Michael Ferguson,&nbsp;Francis Pagani,&nbsp;Paul C. Tang,&nbsp;David Nordsletten","doi":"10.1007/s10237-026-02063-9","DOIUrl":"10.1007/s10237-026-02063-9","url":null,"abstract":"<div><p>We present a fully coupled, patient-specific 3D–0D computational framework for hearts supported with left ventricular assist devices (LVAD) that enables controlled <i>in silico</i> experimentation. The approach monolithically integrates three-dimensional CFD of the left ventricle (LV), left atrium (LA), aortic root, and LVAD cannulae with a closed-loop 0D lumped parameter network of the full circulation. Mitral and aortic valve dynamics are governed by transvalvular pressure and flow with patient-specific regurgitant orifice areas, and the LVAD is represented via a pressure–flow (H–Q) relation. This manuscript provides the complete mathematical formulation, coupling strategy, and parameterization required to build a reproducible pipeline from dynamic CT, 2D transthoracic echocardiography, and right heart catheterization. This methodology is demonstrated in a patient under long-term support of LVAD and concomitant mitral and aortic regurgitation. The personalized, fully coupled 3D–0D models reproduced available clinical targets with a mean error of 8.6%, enabling controlled <i>in silico</i> interrogation of valve repair strategies. In the patient-specific state, simulated mitral and aortic regurgitant volumes were 6.6 and 6.5 mL per cycle, yielding a forward cardiac output of 3.16 L/min despite an LVAD flow of 3.7 L/min. In silico isolated mitral valve (MV) repair, isolated aortic valve (AV) repair, and combined MV+AV repair increased forward output to 3.41, 3.33, and 3.55 L/min, respectively; however, aortic valve opening and increased aortic pressure pulsatility (up to 38.9 vs. 13.5 mmHg) were observed only when MV repair was involved. These left-sided improvements propagated through the cardiopulmonary circulation, reducing pulmonary pressures and right ventricular loading, with the largest benefit observed following combined repair. We show that the modeling platform presented provides a powerful means to study mechanical circulatory support, enabling patient-specific evaluation of surgical interventions in patients with LVAD and delivering quantitative insight into clinically important metrics—such as aortic pulsatility, RV afterload, and chamber-level flow patterns.\u0000</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02063-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148147951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modification of a poroelastic model for zero porosity: finite element implementation and investigation of fluid mechanics in the perivascular space","authors":"Mohammad Jannesari,&nbsp;Beatrice Ghitti,&nbsp;Bruce J. Gluckman,&nbsp;Francesco Costanzo","doi":"10.1007/s10237-026-02070-w","DOIUrl":"10.1007/s10237-026-02070-w","url":null,"abstract":"<div><p>In conventional formulations of poroelasticity, when the porosity approaches zero or vanishes in some parts of the poroelastic domain, if only temporarily, the governing equations degenerate to those for the solid phase thereby inhibiting a suitable determination of the fluid velocity field. To address this challenge, we reformulated a poroelastic model based on mixture theory to accommodate scenarios with zero porosity. We verified our model using the method of manufactured solutions and demonstrated its ability to handle extreme conditions in a sample test problem. As an application of our framework, we investigated peristaltic flow in the perivascular space of a penetrating arteriole in brain. Our analysis revealed that some literature-suggested parameters can drive the model to predict extreme non-physiological conditions. We further demonstrated that these extreme conditions can be somewhat mitigated by accounting for the deformation of the surrounding brain tissue.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02070-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of inflammatory response in secondary brain injury: a review of computational approaches, challenges, and future directions","authors":"Fatemeh Jafarabadi,&nbsp;Meenal Datta,&nbsp;Maria A. Holland","doi":"10.1007/s10237-026-02074-6","DOIUrl":"10.1007/s10237-026-02074-6","url":null,"abstract":"<div><p>Traumatic brain injury (TBI) and the resulting brain damage and dysfunction are one of the leading causes of death for individuals under 40 worldwide. TBI can occur due to any external force causing deformation in the brain, and it involves a complicated timeline of the initial mechanical damage followed by a subsequent inflammatory response. The details and extent of the effects of TBI on the brain are understudied; however, researchers have developed a vast array of experimental and computational models in order to investigate the complex physiological dynamics and interactions in TBI. This review summarizes the hallmarks of TBI, focusing on the inflammatory response mechanisms within the secondary injury and how they have been modeled computationally. Finally, we highlight potential areas of improvement for computational models of TBI to enhance their relevance for translational and clinical research.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02074-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148147965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}