0


Guest Editorial

J Biomech Eng. 2019;141(9):090301-090301-1. doi:10.1115/1.4044065.
FREE TO VIEW

This September we celebrate the 100th birthday of Professor Y. C. Fung, the Father of Biomechanics. There are multiple events organized in the biomechanics and biomedical engineering communities in honor of Professor Fung, including the YC Fung symposium at the Summer Biomechanics, Bioengineering and Biotransport Conference (SB3C2019) in Seven Spring, PA in June and the YC Fung symposium at San Diego, CA in September. A special issue has been published by the Journal of Medical Biomechanics [1]. The ASME Journal of Biomechanical Engineering organized this special issue titled “Special Issue: A Tribute to Dr. Y. C Fung,” to celebrate Dr. Fung's birthday and his contributions to science and engineering.

Commentary by Dr. Valentin Fuster

Review Article

J Biomech Eng. 2019;141(9):090801-090801-7. doi:10.1115/1.4043434.
FREE TO VIEW

Cardioprotective engineering is an emerging bioengineering discipline aiming to develop engineering strategies to optimize cardioprotective actions against cardiac injuries and disorders. Although there exist innate cardioprotective mechanisms capable of supporting cardiomyocyte survival in response to an insult, not all these mechanisms are optimized in promptness and effectiveness, suggesting the necessity of cardioprotective engineering. Various cardioprotective strategies have been developed and used in experimental and clinical investigations; however, few of these strategies have exerted a significant clinical impact. There are two major challenges in cardioprotective engineering—understanding the innate cardioprotective mechanisms and developing engineering strategies for precise control of the types, levels, timing, and coordination of cardioprotective actions to facilitate recovery from injuries and disorders. Understanding the innate mechanisms is the foundation for developing cardioprotective engineering strategies. Here, ischemic myocardial injury is used as an example to demonstrate the concept of cardioprotective engineering.

Commentary by Dr. Valentin Fuster

Research Papers

J Biomech Eng. 2019;141(9):091001-091001-9. doi:10.1115/1.4044053.
FREE TO VIEW

Professor Y. C. Fung has made superb contributions to science, engineering, and humanity through his research and its applications, as well as his words and deeds. By setting the highest standards of rigor and excellence, training many outstanding students and their students, and providing his exemplary leadership, Dr. Fung has made tremendous impacts that spread across the world and transcend time. He established the foundations of biomechanics in a variety of living tissues, including the lung, the heart, blood vessels, blood cells, ureter, intestine, skin, as well as other organs and tissues. Through his vision of the power of “making models” to explain and predict biological phenomena, Dr. Fung opened up new horizons for bioengineering, from organs/systems to molecules/genes. He has initiated and fostered the research activities in many institutions in the U.S. and elsewhere in the world. He has made outstanding contributions to education in bioengineering, as well as service to the professional organizations and translation to industry and clinical medicine. He is widely recognized as the Father of Biomechanics and the leading Bioengineer in the world. His extraordinary accomplishments and commands in science, engineering, and the arts make him a Renaissance Man whom the world is most fortunate to have.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091002-091002-11. doi:10.1115/1.4044066.
FREE TO VIEW
Topics: Biomechanics , China
Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091003-091003-9. doi:10.1115/1.4043866.
FREE TO VIEW

Medical image resolution has been a serious limitation in plaque progression research. A modeling approach combining intravascular ultrasound (IVUS) and optical coherence tomography (OCT) was introduced and patient follow-up IVUS and OCT data were acquired to construct three-dimensional (3D) coronary models for plaque progression investigations. Baseline and follow-up in vivo IVUS and OCT coronary plaque data were acquired from one patient with 105 matched slices selected for model construction. 3D fluid–structure interaction (FSI) models based on IVUS and OCT data (denoted as IVUS + OCT model) were constructed to obtain stress/strain and wall shear stress (WSS) for plaque progression prediction. IVUS-based IVUS50 and IVUS200 models were constructed for comparison with cap thickness set as 50 and 200 μm, respectively. Lumen area increase (LAI), plaque area increase (PAI), and plaque burden increase (PBI) were chosen to measure plaque progression. The least squares support vector machine (LS-SVM) method was employed for plaque progression prediction using 19 risk factors. For IVUS + OCT model with LAI, PAI, and PBI, the best single predictor was plaque strain, local plaque stress, and minimal cap thickness, with prediction accuracy as 0.766, 0.838, and 0.890, respectively; the prediction accuracy using best combinations of 19 factors was 0.911, 0.881, and 0.905, respectively. Compared to IVUS + OCT model, IVUS50, and IVUS200 models had errors ranging from 1% to 66.5% in quantifying cap thickness, stress, strain and prediction accuracies. WSS showed relatively lower prediction accuracy compared to other predictors in all nine prediction studies.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091004-091004-12. doi:10.1115/1.4043486.
OPEN ACCESS

Findings from basic science and clinical studies agree that arterial stiffness is fundamental to both the mechanobiology and the biomechanics that dictate vascular health and disease. There is, therefore, an appropriately growing literature on arterial stiffness. Perusal of the literature reveals, however, that many different methods and metrics are used to quantify arterial stiffness, and reported values often differ by orders of magnitude and have different meanings. Without clear definitions and an understanding of possible inter-relations therein, it is increasingly difficult to integrate results from the literature to glean true understanding. In this paper, we briefly review methods that are used to infer values of arterial stiffness that span studies on isolated cells, excised intact vessels, and clinical assessments. We highlight similarities and differences and identify a single theoretical approach that can be used across scales and applications and thus could help to unify future results. We conclude by emphasizing the need to move toward a synthesis of many disparate reports, for only in this way will we be able to move from our current fragmented understanding to a true appreciation of how vascular cells maintain, remodel, or repair the arteries that are fundamental to cardiovascular properties and function.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091005-091005-6. doi:10.1115/1.4044227.
FREE TO VIEW

Incompressibility implies that a tissue preserves its volume regardless of the loading conditions. Although this assumption is well-established in arterial wall mechanics, it is assumed to apply for the venous wall without validation. The objective of this study is to test whether the incompressibility assumption holds for the venous wall. To investigate the vascular wall volume under different loading conditions, inflation-extension testing protocol was used in conjunction with intravascular ultrasound (IVUS) in both common iliac arteries (n = 6 swine) and common iliac veins (n = 9 dogs). Use of IVUS allows direct visualizations of lumen dimensions simultaneous with direct measurements of outer dimensions during loading. The arterial tissue was confirmed to preserve volume during various load conditions (p = 0.11) consistent with the literature, while the venous tissue was found to lose volume (about 35%) under loaded conditions (p < 0.05). Using a novel methodology, this study shows the incompressibility assumption does not hold for the venous wall especially at higher pressures, which suggests that there may be fluid loss through the vein wall during loading. This has important implications for coupling of fluid transport across the wall and biomechanics of the wall in healthy and diseased conditions.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091006-091006-12. doi:10.1115/1.4044046.
FREE TO VIEW

Blood pressure is an important factor both in maintaining body homeostasis and in its disruption. Vascular endothelial cells (ECs) are exposed to varying degrees of blood pressure and therefore play an important role in these physiological and pathological events. However, the effect of blood pressure on EC functions remains to be elucidated. In particular, we do not know how ECs sense and respond to changes in hydrostatic pressure even though the hydrostatic pressure is known to affect the EC functions. Here, we hypothesized that the cellular responses, leading to the reported pressure effects, occur at an early stage of pressure exposure and observed the early-stage dynamics in ECs to elucidate mechanisms through which ECs sense and respond to hydrostatic pressure. We found that exposure to hydrostatic pressure causes an early actomyosin-mediated contraction of ECs without a change in cell morphology. This response could be caused by water efflux from the ECs following exposure to hydrostatic pressure. Although only a limited study, these findings do explain a part of the mechanism through which ECs sense and respond to hydrostatic pressure.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091007-091007-10. doi:10.1115/1.4044215.
FREE TO VIEW

We sought to calibrate mechanical properties of left ventricle (LV) based on three-dimensional (3D) speckle tracking echocardiographic imaging data recorded from 16 segments defined by American Heart Association (AHA). The in vivo data were used to create finite element (FE) LV and biventricular (BV) models. The orientation of the fibers in the LV model was rule based, but diffusion tensor magnetic resonance imaging (MRI) data were used for the fiber directions in the BV model. A nonlinear fiber-reinforced constitutive equation was used to describe the passive behavior of the myocardium, whereas the active tension was described by a model based on tissue contraction (Tmax). isight was used for optimization, which used abaqus as the forward solver (Simulia, Providence, RI). The calibration of passive properties based on the end diastolic pressure volume relation (EDPVR) curve resulted in relatively good agreement (mean error = −0.04 ml). The difference between the experimental and computational strains decreased after segmental strain metrics, rather than global metrics, were used for calibration: for the LV model, the mean difference reduced from 0.129 to 0.046 (circumferential) and from 0.076 to 0.059 (longitudinal); for the BV model, the mean difference nearly did not change in the circumferential direction (0.061) but reduced in the longitudinal direction from 0.076 to 0.055. The calibration of mechanical properties for myocardium can be improved using segmental strain metrics. The importance of realistic fiber orientation and geometry for modeling of the LV was shown.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091008-091008-7. doi:10.1115/1.4044175.
FREE TO VIEW

High-resolution peripheral quantitative computed tomography (HR-pQCT) is a promising imaging modality that provides an in vivo three-dimensional (3D) assessment of bone microstructure by scanning fixed regions of the distal radius and tibia. However, how microstructural parameters and mechanical analysis based on these segment scans correlate to whole distal radius and tibia mechanics are not well-characterized. On 26 sets of cadaveric radius and tibia, HR-pQCT scans were performed on the standard scan segment, a segment distal to the standard segment, and a segment proximal to the standard segment. Whole distal radius and tibia stiffness were determined through mechanical testing. Segment bone stiffness was estimated using linear finite element (FE) analysis based on segment scans. Standard morphological and individual trabecula segmentation (ITS) analyses were used to estimate microstructural properties. Significant variations in microstructural parameters were observed among segments at both sites. Correlation to whole distal radius and tibia stiffness was moderate for microstructural parameters at the standard segment, but correlation was significantly increased for FE-predicted segment bone stiffness based on standard segment scans. Similar correlation strengths were found between FE-predicted segment bone stiffness and whole distal radius and tibia stiffness. Additionally, microstructural parameters at the distal segment had higher correlation to whole distal radius and tibia stiffness than at standard or proximal segments. Our results suggest that FE-predicted segment stiffness is a better predictor of whole distal radius and tibia stiffness for clinical HR-pQCT analysis and that microstructural parameters at the distal segment are more highly correlated with whole distal radius and tibia stiffness than at the standard or proximal segments.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091009-091009-11. doi:10.1115/1.4044052.
FREE TO VIEW

Eardrum or tympanic membrane (TM) is a multilayer soft tissue membrane located at the end of the ear canal to receive sound pressure and transport the sound into the middle ear and cochlea. Recent studies reported that the TM microstructure and mechanical properties varied after the ear was exposed to blast overpressure. However, the impact of such biomechanical changes of the TM on its movement for sound transmission has not been investigated. This paper reports the full-field surface motion of the human TM using the scanning laser Doppler vibrometry in human temporal bones under normal and postblast conditions. An increase of the TM displacement after blast exposure was observed in the posterior region of the TM in four temporal bone samples at the frequencies between 3 and 4 kHz. A finite element model of human TM with multilayer microstructure and orthogonal fiber network was created to simulate the TM damaged by blast waves. The consistency between the experimental data and the model-derived TM surface motion suggests that the tissue injuries were resulted from a combination of mechanical property change and regional discontinuity of collagen fibers. This study provides the evidences of surface motion changes of the TM damaged by blast waves and possible fiber damage locations.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091010-091010-10. doi:10.1115/1.4043867.
FREE TO VIEW

Patients who survive a myocardial infarction (MI) are at high risk for ventricular dilation and heart failure. While infarct size is an important determinant of post-MI remodeling, different patients with the same size infarct often display different levels of left ventricular (LV) dilation. The acute physiologic response to MI involves reflex compensation, whereby increases in heart rate (HR), arterial resistance, venoconstriction, and contractility of the surviving myocardium act to maintain mean arterial pressure (MAP). We hypothesized that variability in reflex compensation might underlie some of the reported variability in post-MI remodeling, a hypothesis that is difficult to test using experimental data alone because some reflex responses are difficult or impossible to measure directly. We, therefore, employed a computational model to estimate the balance of compensatory mechanisms from experimentally reported hemodynamic data. We found a strikingly wide range of compensatory reflex profiles in response to MI in dogs and verified that pharmacologic blockade of sympathetic and parasympathetic reflexes nearly abolished this variability. Then, using a previously published model of postinfarction remodeling, we showed that observed variability in compensation translated to variability in predicted LV dilation consistent with published data. Treatment with a vasodilator shifted the compensatory response away from arterial and venous vasoconstriction and toward increased HR and myocardial contractility. Importantly, this shift reduced predicted dilation, a prediction that matched prior experimental studies. Thus, postinfarction reflex compensation could represent both a source of individual variability in the extent of LV remodeling and a target for therapies aimed at reducing that remodeling.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091011-091011-8. doi:10.1115/1.4044225.
FREE TO VIEW

Pulmonary arterial hypertension (PAH) commonly leads to right ventricular (RV) hypertrophy and fibrosis that affect the mechanical properties of the RV myocardium (MYO). To investigate the effects of PAH on the mechanics of the RV MYO and extracellular matrix (ECM), we compared RV wall samples, isolated from rats in which PAH was induced using the SuHx protocol, with samples from control animals before and after the tissues were decellularized. Planar biaxial mechanical testing, a technique first adapted to living soft biological tissues by Fung, was performed on intact and decellularized samples. Fung's anisotropic exponential strain energy function fitted the full range of biaxial test results with high fidelity in control and PAH samples both before and after they were decellularized. Mean RV myocardial apex-to-outflow tract and circumferential stresses during equibiaxial strain were significantly greater in PAH than control samples. Mean RV ECM circumferential but not apex-to-outflow tract stresses during equibiaxial strain were significantly greater in the PAH than control group. The ratio of ECM to myocardial stresses at matched strains did not change significantly between groups. Circumferential stresses were significantly higher than apex-to-outflow tract stresses for all groups. These findings confirm the predictions of a mathematical model based on changes in RV hemodynamics and morphology in rat PAH, and may provide a foundation for a new constitutive analysis of the contributions of ECM remodeling to changes in RV filling properties during PAH.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091012-091012-9. doi:10.1115/1.4044214.
FREE TO VIEW

Endovascular coil embolization is now widely used to treat cerebral aneurysms (CA) as an alternative to surgical clipping. It involves filling the aneurysmal sac with metallic coils to reduce flow, induce clotting, and promote the formation of a coil/thrombus mass which protects the aneurysm wall from hemodynamic forces and prevents rupture. However, a significant number of aneurysms are incompletely coiled leading to aneurysm regrowth and/or recanalization. Computational models of aneurysm coiling may provide important new insights into the effects of intrasaccular coil and thrombus on aneurysm wall stresses. Porcine blood and platinum coils were used to construct an in vitro coil thrombus mass (CTM) for mechanical testing. A uniaxial compression test was performed with whole blood clots and CTM, with coil packing densities (CPDs) of 10%, 20%, and 30% to obtain compressive stress/strain responses. A fourth-order polynomial mechanical response function was fit to the experimentally obtained stress/strain responses for each CPD in order to represent their mechanical properties for computational simulations. Patient-specific three-dimensional (3D) geometries of three aneurysms with simple geometry and four with complex geometry were reconstructed from digital subtraction angiography (DSA) images. The CPDs were digitally inserted in the aneurysm geometries and finite element modeling was used to determine transmural peak/mean wall stress (MWS) with and without coil packing. Reproducible stress/strain curves were obtained from compression testing of CTM and the polynomial mechanical response function was found to approximate the experimental stress/strain relationship obtained from mechanical testing to a high degree. An exponential increase in the CTM stiffness was observed with increasing CPD. Elevated wall stresses were found throughout the aneurysm dome, neck, and parent artery in simulations of the CAs with no filling. Complete, 100% filling of the aneurysms with whole blood clot and CPDs of 10%, 20%, and 30% significantly reduced MWS in simple and complex geometry aneurysms. Sequential increases in CPD resulted in significantly greater increases in MWS in simple but not complex geometry aneurysms. This study utilizes finite element analysis to demonstrate the reduction of transmural wall stress following coil embolization in patient-specific computational models of CAs. Our results provide a quantitative measure of the degree to which CPD impacts wall stress and suggest that complex aneurysmal geometries may be more resistant to coil embolization treatment. The computational modeling employed in this study serves as a first step in developing a tool to evaluate the patient-specific efficacy of coil embolization in treating CAs.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091013-091013-12. doi:10.1115/1.4044051.
FREE TO VIEW

Abnormal loading of a joint's ligamentous capsule causes pain by activating the capsule's nociceptive afferent fibers, which reside in the capsule's collagenous matrix alongside fibroblast-like synoviocytes (FLS) and transmit pain to the dorsal root ganglia (DRG). This study integrated FLS into a DRG-collagen gel model to better mimic the anatomy and physiology of human joint capsules; using this new model, the effect of FLS on multiscale biomechanics and cell physiology under load was investigated. Primary FLS cells were co-cultured with DRGs at low or high concentrations, to simulate variable anatomical FLS densities, and failed in tension. Given their roles in collagen degradation and nociception, matrix-metalloproteinase (MMP-1) and neuronal expression of the neurotransmitter substance P were probed after gel failure. The amount of FLS did not alter (p > 0.3) the gel failure force, displacement, or stiffness. FLS doubled regional strains at both low (p < 0.01) and high (p = 0.01) concentrations. For high FLS, the collagen network showed more reorganization at failure (p < 0.01). Although total MMP-1 and neuronal substance P were the same regardless of FLS concentration before loading, protein expression of both increased after failure, but only in low FLS gels (p ≤ 0.02). The concentration-dependent effect of FLS on microstructure and cellular responses implies that capsule regions with different FLS densities experience variable microenvironments. This study presents a novel DRG-FLS co-culture collagen gel system that provides a platform for investigating the complex biomechanics and physiology of human joint capsules, and is the first relating DRG and FLS interactions between each other and their surrounding collagen network.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091014-091014-10. doi:10.1115/1.4043831.
FREE TO VIEW

Trabeculae carneae are irregular structures that cover the endocardial surfaces of both ventricles and account for a significant portion of human ventricular mass. The role of trabeculae carneae in diastolic and systolic functions of the left ventricle (LV) is not well understood. Thus, the objective of this study was to investigate the functional role of trabeculae carneae in the LV. Finite element (FE) analyses of ventricular functions were conducted for three different models of human LV derived from high-resolution magnetic resonance imaging (MRI). The first model comprised trabeculae carneae and papillary muscles, while the second model had papillary muscles and partial trabeculae carneae, and the third model had a smooth endocardial surface. We customized these patient-specific models with myofiber architecture generated with a rule-based algorithm, diastolic material parameters of Fung strain energy function derived from biaxial tests and adjusted with the empirical Klotz relationship, and myocardial contractility constants optimized for average normal ejection fraction (EF) of the human LV. Results showed that the partial trabeculae cutting model had enlarged end-diastolic volume (EDV), reduced wall stiffness, and even increased end-systolic function, indicating that the absence of trabeculae carneae increased the compliance of the LV during diastole, while maintaining systolic function.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091015-091015-9. doi:10.1115/1.4043865.
FREE TO VIEW

The scar that forms after a myocardial infarction is often characterized by a highly disordered architecture but generally exhibits some degree of collagen fiber orientation, with a resulting mechanical anisotropy. When viewed in finer detail, however, the heterogeneity of the sample is clear, with different subregions exhibiting different fiber orientations. In this work, we used a multiscale finite element model to explore the consequences of the heterogeneity in terms of mechanical behavior. To do so, we used previously obtained fiber alignment maps of rat myocardial scar slices (n = 15) to generate scar-specific finite element meshes that were populated with fiber models based on the local alignment state. These models were then compared to isotropic models with the same sample shape and fiber density, and to homogeneous models with the same sample shape, fiber density, and average fiber alignment as the scar-specific models. All simulations involved equibiaxial extension of the sample with free motion in the third dimension. We found that heterogeneity led to a lower degree of mechanical anisotropy and a higher level of local stress concentration than the corresponding homogeneous model, and also that fibers failed in the heterogeneous model at much lower macroscopic strains than in the isotropic and homogeneous models. Taken together, these results suggest that scar heterogeneity may impair myocardial mechanical function both in terms of anisotropy and strength, and that individual variations in scar heterogeneity could be an important consideration for understanding scar remodeling and designing therapeutic interventions for patients after myocardial infarction.

Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091016-091016-13. doi:10.1115/1.4044174.
FREE TO VIEW

Pulmonary arterial hypertension (PAH) exerts substantial pressure overload on the right ventricle (RV), inducing RV remodeling and myocardial tissue adaptation often leading to right heart failure. The associated RV free wall (RVFW) adaptation involves myocardial hypertrophy, augmented intrinsic contractility, collagen fibrosis, and structural remodeling in an attempt to cope with pressure overload. If RVFW adaptation cannot maintain the RV stroke volume (SV), RV dilation will prevail as an exit mechanism, which usually decompensates RV function, leading to RV failure. Our knowledge of the factors determining the transition from the upper limit of RVFW adaptation to RV decompensation and the role of fiber remodeling events such as extracellular fibrosis and fiber reorientation in this transition remains very limited. Computational heart models that connect the growth and remodeling (G&R) events at the fiber and tissue levels with alterations in the organ-level function are essential to predict the temporal order and the compensatory level of the underlying mechanisms. In this work, building upon our recently developed rodent heart models (RHM) of PAH, we integrated mathematical models that describe volumetric growth of the RV and structural remodeling of the RVFW. The time-evolution of RV remodeling from control and post-PAH time points was simulated. The results suggest that the augmentation of the intrinsic contractility of myofibers, accompanied by an increase in passive stiffness of RVFW, is among the first remodeling events through which the RV strives to maintain the cardiac output. Interestingly, we found that the observed reorientation of the myofibers toward the longitudinal (apex-to-base) direction was a maladaptive mechanism that impaired the RVFW contractile pattern and advanced along with RV dilation at later stages of PAH. In fact, although individual fibers were more contractile post-PAH, the disruption in the optimal transmural fiber architecture compromised the effective contractile function of the RVFW, contributing to the depressed ejection fraction (EF) of the RV. Our findings clearly demonstrate the critical need for developing multiscale approaches that can model and delineate relationships between pathological alterations in cardiac function and underlying remodeling events across fiber, cellular, and molecular levels.

Topics: Fibers , Pressure
Commentary by Dr. Valentin Fuster
J Biomech Eng. 2019;141(9):091017-091017-13. doi:10.1115/1.4043977.
FREE TO VIEW

The cervix is essential to a healthy pregnancy as it must bear the increasing load caused by the growing fetus. Preterm birth is suspected to be caused by the premature softening and mechanical failure of the cervix. The objective of this paper is to measure the anisotropic mechanical properties of human cervical tissue using indentation and video extensometry. The human cervix is a layered structure, where its thick stromal core contains preferentially aligned collagen fibers embedded in a soft ground substance. The fiber composite nature of the tissue provides resistance to the complex three-dimensional loading environment of pregnancy. In this work, we detail an indentation mechanical test to obtain the force and deformation response during loading which closely matches in vivo conditions. We postulate a constitutive material model to describe the equilibrium material behavior to ramp-hold indentation, and we use an inverse finite element method based on genetic algorithm (GA) optimization to determine best-fit material parameters. We report the material properties of human cervical slices taken at different anatomical locations from women of different obstetric backgrounds. In this cohort of patients, the anterior internal os (the area where the cervix meets the uterus) of the cervix is stiffer than the anterior external os (the area closest to the vagina). The anatomic anterior and posterior quadrants of cervical tissue are more anisotropic than the left and right quadrants. There is no significant difference in material properties between samples of different parities (number of pregnancies reaching viable gestation age).

Commentary by Dr. Valentin Fuster

Technical Brief

J Biomech Eng. 2019;141(9):094501-094501-5. doi:10.1115/1.4044134.
FREE TO VIEW

A mechanical approach is needed for understanding anorectal function and defecation. Fecal continence is achieved by several interacting mechanisms including anatomical factors, anorectal sensation, rectal compliance, stool consistency, anal muscle strength, motility, and psychological factors. The balance is easily disturbed, resulting in symptoms such as fecal incontinence and constipation. Novel technologies have been developed in recent years for studying anorectal function. Especially, the Fecobionics device, a simulated feces, has gained attention recently. This facilitates new analysis of anorectal mechanical function. In this study, a theoretical model is developed to analyze anorectal mechanophysiological data generated by the Fecobionics device. Theoretical approaches can enhance future interdisciplinary research for unraveling defecatory function, sensory-motor disorders, and symptoms. This is a step in the direction of personalized treatment for gastrointestinal disorders based on optimized subtyping of anorectal disorders.

Commentary by Dr. Valentin Fuster

Sorry! You do not have access to this content. For assistance or to subscribe, please contact us:

  • TELEPHONE: 1-800-843-2763 (Toll-free in the USA)
  • EMAIL: asmedigitalcollection@asme.org
Sign In