Molecular & Cellular Biomechanics

ISSN: 1556-5297 (printed)
ISSN: 1556-5300 (online) Publication Frequency: Quarterly

About the journal

The field of biomechanics concerns with motion, deformation, and forces in biological systems. With the explosive progress in molecular biology, genomic engineering, bioimaging, and nanotechnology, there will be an ever-increasing generation of knowledge and information concerning the mechanobiology of genes, proteins, cells, tissues, and organs. Such information will bring new diagnostic tools, new therapeutic approaches, and new knowledge on ourselves and our interactions with our environment. It becomes apparent that biomechanics focusing on molecules, cells as well as tissues and organs is an important aspect of modern biomedical sciences. The aims of this journal are to facilitate the studies of the mechanics of biomolecules (including proteins, genes, cytoskeletons, etc.), cells (and their interactions with extracellular matrix), tissues and organs, the development of relevant advanced mathematical methods, and the discovery of biological secrets. As science concerns only with relative truth, we seek ideas that are state-of-the-art, which may be controversial, but stimulate and promote new ideas, new techniques, and new applications. This journal will encourage the exchange of ideas that may be seminal, or hold promise to stimulate others to new findings.

Indexing and Abstracting

Applied Mechanics Reviews; BIOBASE (Elsevier); BIOSIS Preview-Web of Science (Clarivate Analytics); Cambridge Scientific Abstracts-Proquest; Ei Compendex / Engineering Village (Elsevier); EMBASE (Elsevier); GEOBASE (Elsevier); INSPEC (IET); Science Navigator; Scopus (Elsevier): Citescore 2018: 0.64; SNIP (Source Normalized Impact per Paper 2018): 0.528; World Textiles and Scopus; Zentralblatt fur Mathematik; Portico, etc...

Current Issue - Vol.17, No.1, 2020 Most Viewed

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RESEARCH ARTICLE
On the Onset of Cracks in Arteries¹
P. Mythravaruni, K.Y. Volokh^*
Molecular & Cellular Biomechanics, Vol.17, No.1, pp. 1-17, 2020, DOI:10.32604/mcb.2019.07606
Abstract We present a theoretical approach to study the onset of failure localization into cracks in arterial wall. The arterial wall is a soft composite comprising hydrated ground matrix of proteoglycans reinforced by spatially dispersed elastin and collagen fibers. As any material, the arterial tissue cannot accumulate and dissipate strain energy beyond a critical value. This critical value is enforced in the constitutive theory via energy limiters. The limiters automatically bound reachable stresses and allow examining the mathematical condition of strong ellipticity. Loss of the strong ellipticity physically means inability of material to propagate superimposed waves. The waves cannot propagate because material failure localizes into cracks perpendicular to a possible wave direction. Thus, not only the onset of a crack can be analyzed but also its direction. We use the recently developed constitutive theories of the arterial wall including 8 and 16 structure tensors to account for the fiber dispersion. We enhance these theories with energy limiters. We examine the loss of strong ellipticity in uniaxial tension and pure shear in circumferential and axial directions of the arterial wall. We find that the vanishing longitudinal wave speed predicts the appearance of cracks in the direction perpendicular to tension. We also find that the vanishing transverse wave speed predicts the appearance of cracks in the the direction inclined (non-perpendicular) to tension. The latter result is counter-intuitive yet it is supported by recent experimental observations.
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Kinematic and Dynamic Characteristics of Pulsating Flow in 180^o Tube
Tin-Kan Hung^1,*, Ruei-Hung Kuo², Cheng-Hsien Chiang³
Molecular & Cellular Biomechanics, Vol.17, No.1, pp. 19-24, 2020, DOI:10.32604/mcb.2019.07817
Abstract Kinematic and dynamic characteristics of pulsating flow in a model of human aortic arch are obtained by a computational analysis. Three-dimensional flow processes are summarized by pressure distributions on the symmetric plane together with velocity and pressure contours on a few cross sections for systolic acceleration and deceleration. Without considering the effects of aortic tapering and the carotid arteries, the development of tubular boundary layer with centrifugal forces and pulsation are also analyzed for flow separation and backflow during systolic deceleration.
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New Concept in Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA)
Ali. E. Dabiri^1,2,*, Matthew Martin³, Ghassan S. Kassab¹
Molecular & Cellular Biomechanics, Vol.17, No.1, pp. 25-31, 2020, DOI:10.32604/mcb.2019.07310
Abstract The world-wide impact of traumatic injury and associated hemorrhage on human health and well-being is significant. Methods to manage bleeding from sites within the torso, referred to as non-compressible torso hemorrhage (NCTH), remain largely limited to the use of conventional operative techniques. The overall mortality rate of patients with NCTH is approximately 50%. Studies from the wars in Afghanistan and Iraq have suggested that up to 80% of potentially survivable patients die as a result of uncontrolled exsanguinating hemorrhage. The commercially available resuscitative endovascular balloon occlusion of the aorta (REBOA) is a percutaneous device for the rapid control of torso hemorrhage in trauma. A compliant balloon is inserted via the femoral artery and inflated in the thoracic or abdominal aorta, providing inflow control of the abdomen, pelvis, or groin/lower extremities. Recent studies indicate that REBOA carries an inherent risk of aortic injury due to over-inflation and possible risk of aortic or iliac artery rupture. A new approach isto resolve the issue of balloon sizing and over-inflation. We propose a novel concept to be used in trauma facility for arterial occlusion to eliminate arterial injury and the risk of vascular rupture through real time balloon diameter profile measurements to ensure proper inflation. The proposed concept, called Smart Resuscitative Endovascular Balloon Occlusion (SREBO) will be novel in the following aspects: 1) It will have electrical conductance-based navigation technology to target the desired site of balloon deployment in the aorta, 2) The balloon can determine the time of proper inflation using electrical conductance catheter technology. This technology would eliminate the risk of arterial rupture and simplify the procedure in the trauma facility or medical clinics without significant training. The results can be displayed on a handheld device. This novel device has the potential to save civilians in trauma or soldiers injured on the battlefield.
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Multifrequency Microwave Imaging for Brain Stroke Detection
Lulu Wang^1,*
Molecular & Cellular Biomechanics, Vol.17, No.1, pp. 33-40, 2020, DOI:10.32604/mcb.2019.07165
Abstract CT and MRI are often used in the diagnosis and monitoring of stroke. However, they are expensive, time-consuming, produce ionizing radiation (CT), and not suitable for continuous monitoring stroke. Microwave imaging (MI) has been extensively investigated for identifying several types of human organs, including breast, brain, lung, liver, and gastric. The authors recently developed a holographic microwave imaging (HMI) algorithm for biological object detection. However, this method has difficulty in providing accurate information on embedded small inclusions. This paper describes the feasibility of the use of a multifrequency HMI algorithm for brain stroke detection. A numerical system, including HMI data collection model and a realistic head model, was developed to demonstrate the proposed method for imaging of brain tissues. Various experiments were carried out to evaluate the performance of the proposed method. Results of experiments carried out using multifrequency HMI have been compared with the results obtained from single frequency HMI. Results showed that multifrequency HMI could detect strokes and provide more accurate results of size and location than the single frequency HMI algorithm.
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A Retrospective Respiratory Gating System Based on Epipolar Consistency Conditions
Maosen Lian¹, Yi Li¹, Xiaohui Gu¹, Shouhua Luo^1,*
Molecular & Cellular Biomechanics, Vol.17, No.1, pp. 41-48, 2020, DOI:10.32604/mcb.2019.07383
Abstract Motion artifacts of in vivo imaging, due to rapid respiration rate and respiration displacements of the mice while free-breathing, is a major challenge in micro computed tomography(micro-CT). The respiratory gating is often served for either projective images acquisition or per projection qualification, so as to eliminate the artifacts brought by in vivo motion. In this paper, we propose a novel respiratory gating method, which firstly divides one rotation cycle into a number of segments, and extracts the respiratory signal from the projective image series of current segment by the value of the epipolar consistency conditions (ECC), then in terms of the measured average respiratory period, sets next segment’s start-up time and rotation speed of the gantry for respiratory phase synchronization, and so on so forth. The gating procedure is through the whole projections of three cycles, only one among three projections at each angle is qualified by their phase value and is retained for future use for tomographic image reconstruction. In practical experiment, the ECC based gating method and the conventional hardware gating method are employed on micro CT imaging of C57BL/6 mice respectively. The result shows that, compared with the hardware based one, the proposed method not only achieve much better consistency in the projection images, but also suppresses the streak artifacts more effectively on the different parts like the breast, abdomen and head of in vivo mice.
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A Study on the Finite Element Model for Head Injury in Facial Collision Accident
Bin Yang^1,2,3,*, Hao Sun¹, Aiyuan Wang¹, Qun Wang²
Molecular & Cellular Biomechanics, Vol.17, No.1, pp. 49-62, 2020, DOI:10.32604/mcb.2019.07534
Abstract In order to predict and evaluate injury mechanism and biomechanical response of the facial impact on head injury in a crash accident. With the combined modern medical imaging technologies, namely computed tomography (CT) and magnetic resonance imaging (MRI), both geometric and finite element (FE) models for human head-neck with detailed cranio-facial structure were developed. The cadaveric head impact tests were conducted to validate the headneck finite element model. The intracranial pressure, skull dynamic response and skull-brain relative displacement of the whole head-neck model were compared with experimental data. Nine typical cases of facial traffic accidents were simulated, with the individual stress wave propagation paths to the intracranial contents through the facial and cranial skeleton being discussed thoroughly. Intracranial pressure, von Mises stress and shear stress distribution were achieved. It is proved that facial structure dissipates a large amount of impact energy to protect the brain in its most natural way. The propagation path and distribution of stress wave in the skull and brain determine the mechanism of brain impact injury, which provides a theoretic basis for the diagnosis, treatment and protection of craniocerebral injury caused by facial impact.
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Traction Force Measurements of Human Aortic Smooth Muscle Cells Reveal a Motor-Clutch Behavior
Petit Claudie¹, Guignandon Alain², Avril Stéphane^1,*
Molecular & Cellular Biomechanics, Vol.16, No.2, pp. 87-108, 2019, DOI:10.32604/mcb.2019.06415
Abstract The contractile behavior of smooth muscle cells (SMCs) in the aorta is an important determinant of growth, remodeling, and homeostasis. However, quantitative values of SMC basal tone have never been characterized precisely on individual SMCs. Therefore, to address this lack, we developed an in vitro technique based on Traction Force Microscopy (TFM). Aortic SMCs from a human lineage at low passages (4-7) were cultured 2 days in conditions promoting the development of their contractile apparatus and seeded on hydrogels of varying elastic modulus (1, 4, 12 and 25 kPa) with embedded fluorescent microspheres. After complete adhesion, SMCs were artificially detached from the gel by trypsin treatment. The microbeads movement was tracked and the deformation fields were processed with a mechanical model, assuming linear elasticity, isotropic material, plane strain, to extract the traction forces formerly applied by individual SMCs on the gel. Two major interesting and original observations about SMC traction forces were deduced from the obtained results: 1. they are variable but driven by cell dynamics and show an exponential distribution, with 40% to 80% of traction forces in the range 0-10 μN. 2. They depend on the substrate stiffness: the fraction of adhesion forces below 10 μN tend to decrease when the substrate stiffness increases, whereas the fraction of higher adhesion forces increases. As these two aspects of cell adhesion (variability and stiffness dependence) and the distribution of their traction forces can be predicted by the probabilistic motor-clutch model, we conclude that this model could be applied to SMCs. Further studies will consider stimulated contractility and primary culture of cells extracted from aneurysmal human aortic tissue.
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Substrate Modulation of Osteoblast Adhesion Strength, Focal Adhesion Kinase Activation, and Responsiveness to Mechanical Stimuli
E. Takai¹, R. Landesberg², R.W. Katz², C.T. Hung³, X.E Guo^1,4
Molecular & Cellular Biomechanics, Vol.3, No.1, pp. 1-12, 2006, DOI:10.3970/mcb.2006.003.001
Abstract Osteoblast interactions with extracellular matrix (ECM) proteins are known to influence many cell functions, which may ultimately affect osseointegration of implants with the host bone tissue. Some adhesion-mediated events include activation of focal adhesion kinase, and subsequent changes in the cytoskeleton and cell morphology, which may lead to changes in adhesion strength and cell responsiveness to mechanical stimuli. In this study we examined focal adhesion kinase activation (FAK), F-actin cytoskeleton reorganization, adhesion strength, and osteoblast responsiveness to fluid shear when adhered to type I collagen (ColI), glass, poly-L-lysine (PLL), fibronectin (FN), vitronectin (VN), and serum (FBS). In general, surfaces that bind cells through integrins (FN, VN, FBS) elicited the highest adhesion strength, FAK activation, and F-actin stress fiber formation after both 15 and 60 minutes of adhesion. In contrast, cells attached through non-integrin mediated means (PLL, glass) showed the lowest FAK activation, adhesion strength, and little F-actin stress fiber formation. When subjected to steady fluid shear using a parallel plate flow chamber, osteoblasts plated on FN released significantly more prostaglandin E2 (PGE₂) compared to those on glass. In contrast, PGE₂ release of osteoblasts attached to FN or glass was not different in the absence of fluid shear, suggesting that differences in binding alone are insufficient to alter PGE₂ secretion. The increased adhesion strength as well as PGE₂ secretion of osteoblasts adhered via integrins may be due to increased F-actin fiber formation, which leads to increased cell stiffness.
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REVIEW ARTICLE
Regulation of Vascular Smooth Muscle Cells and Mesenchymal Stem Cells by Mechanical Strain
Kyle Kurpinski^1,2,3, Jennifer Park^1,2,3, Rahul G. Thakar^1,2,3, Song Li^1,2
Molecular & Cellular Biomechanics, Vol.3, No.1, pp. 21-34, 2006, DOI:10.3970/mcb.2006.003.021
Abstract Vascular smooth muscle cells (SMCs) populate in the media of the blood vessel, and play an important role in the control of vasoactivity and the remodeling of the vessel wall. Blood vessels are constantly subjected to hemodynamic stresses, and the pulsatile nature of the blood flow results in a cyclic mechanical strain in the vessel walls. Accumulating evidence in the past two decades indicates that mechanical strain regulates vascular SMC phenotype, function and matrix remodeling. Bone marrow mesenchymal stem cell (MSC) is a potential cell source for vascular regeneration therapy, and may be used to generate SMCs to construct tissue-engineered vascular grafts for blood vessel replacements. In this review, we will focus on the effects of mechanical strain on SMCs and MSCs, e.g., cell phenotype, cell morphology, cytoskeleton organization, gene expression, signal transduction and receptor activation. We will compare the responses of SMCs and MSCs to equiaxial strain, uniaxial strain and mechanical strain in three-dimensional culture. Understanding the hemodynamic regulation of SMC and MSC functions will provide a basis for the development of new vascular therapies and for the construction of tissue-engineered vascular grafts.
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Development of a Gastrointestinal Tract Microscale Cell Culture Analog to Predict Drug Transport
Gretchen J. McAuliffe^*, Jung Yun Chang^†, Raymond P. Glahn^‡, Michael L. Shuler^§
Molecular & Cellular Biomechanics, Vol.5, No.2, pp. 119-132, 2008, DOI:10.3970/mcb.2008.005.119
Abstract Microscale cell culture analogs (μCCAs) are used to study the metabolism and toxicity of a chemical or drug. These in vitro devices are physical replicas of physiologically based pharmacokinetic models that combine microfabrication and cell culture. The goal of this project is to add an independent GI tract μCCA to a multi-chamber chip μCCA representing the primary circulation. The GI tract μCCA consists of two chambers separated by a microporous membrane on which intestinal epithelial cells are cultured. Compounds of interest are pumped through the top chamber, allowing drug to be absorbed through the epithelial layer and circulated into the chip μCCA. The chip and GI tract μCCAs have been used to recreate the toxic effects of acetaminophen. Preliminary results have shown that the GI tract μCCA acts as a barrier to drugs entering the chip, mimicking in vivo function in this regard.
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Mechanical Loading by Fluid Shear Stress Enhances IGF-1 Receptor Signaling in Osteoblasts in A PKC ζ -Dependent Manner
Jason W. Triplett^∗, Rita O’Riley^∗, Kristyn Tekulve^∗, Suzanne M. Norvell^∗, Fredrick M. Pavalko^†
Molecular & Cellular Biomechanics, Vol.4, No.1, pp. 13-26, 2007, DOI:10.3970/mcb.2007.004.013
Abstract Maintenance of optimal bone physiology requires the coordinated activity of osteoclasts that resorb old bone and osteoblasts that deposit new bone. Mechanical loading of bone and the resulting movement of interstitial fluid within the spaces surrounding bone cells is thought to play a key role is maintaining optimal bone mass. One way in which fluid movement may promote bone formation is by enhancing osteoblast survival. We have shown previously that application of fluid flow to osteoblasts in vitro confers a protective effect by inhibiting osteoblast apoptosis (Pavalko et al., 2003, J. Cell Physiol., 194: 194-205). To investigate the cellular mechanisms that regulate the response of osteoblasts to fluid shear stress, we have examined the possible interaction between fluid flow and growth factors in MC3T3-E1 osteoblast-like cells. We found that insulin-like growth factor-I (IGF-I) was significantly more effective at preventing TNF-$\alpha$-induced apoptosis when cells were first subjected to mechanical loading by exposure to either unidirectional or oscillatory fluid flow compared to cells that were maintained in static culture. Additionally, downstream signaling in response to treatment with IGF-I, including ERK and Akt activation, was enhanced in cells that were subjected to fluid flow, compared to cells maintained in static culture. Furthermore, we found that PKC$\zeta$ activity is essential for fluid shear stress sensitization of IGF-IR, since a specific inhibitor of PCK$\zeta$ function blocked the flow-enhanced IGF-I-activated Akt and ERK phosphorylation. Together, our results suggest that fluid shear stress may regulate IGF-I signaling in osteoblasts in a PKC-$\zeta$-dependent manner.
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Systems Neuroprotective Mechanisms in Ischemic Stroke
Shu Q. Liu^*
Molecular & Cellular Biomechanics, Vol.16, No.2, pp. 75-85, 2019, DOI:10.32604/mcb.2019.06920
Abstract Ischemic stroke, although causing brain infarction and neurological deficits, can activate innate neuroprotective mechanisms, including regional mechanisms within the ischemic brain and distant mechanisms from non-ischemic organs such as the liver, spleen, and pancreas, supporting neuronal survival, confining brain infarction, and alleviating neurological deficits. Both regional and distant mechanisms are defined as systems neuroprotective mechanisms. The regional neuroprotective mechanisms involve release and activation of neuroprotective factors such as adenosine and bradykinin, inflammatory responses, expression of growth factors such as nerve growth factors and neurotrophins, and activation and differentiation of resident neural stem cells to neurons and glial cells. The distant neuroprotective mechanisms are implemented by expression and release of endocrine neuroprotective factors such as fibroblast growth factor 21, resistin like molecule γ, and trefoil factor 3 from the liver; brain-derived neurotrophic factor and nerve growth factor from the spleen; and neurotrophin 3 and vascular endothelial growth factor C from the pancreas. Furthermore, ischemic stroke induces mobilization of bone marrow hematopoietic stem cells and endothelial progenitor cells into the circulatory system and brain, contributing to neuroprotection. The regional and distant mechanisms may act in coordination and synergy to protect the ischemic brain from injury and death. This paper addresses these mechanisms and associated signaling networks.
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