Most mammals, including humans, maintain relatively constant internal temperatures despite changes in ambient conditions and fluctuations in internal heat production. To achieve this end, an individual must be able to: 1) protect the internal milieu from external thermal challenges and 2) dissipate excess internally produced heat. Heat is produced as a byproduct of cellular metabolism and is lost to the environment across the body surface. The thermoregulatory challenge is to dissipate excess internally produced heat despite the insulation layers that protect the internal milieu from external thermal influences.

Prosthetic heart valves (PHVs) and other cardiovascular devices induce flow features such as turbulence, stagnation and high shear which do not occur in the native flow, and can lead to hemolysis and thrombosis due to mechanical loading of cells. As an aid to the development of cardiovascular implants, many researchers have attempted to correlate blood damage with macroscopic flow parameters through in vitro testing. The parameters most widely used are the macroscopic viscous shear stress (e.g. Paul et al . [1]) and the macroscopic Reynolds stresses in turbulent flow (e.g. Sallam and Hwang [2]). Although these quantities are valuable predictors of flow induced blood damage, they are not equivalent to the true stresses on a blood cell. In particular, Reynolds stress characterises velocity fluctuations at all length scales; therefore, it cannot completely describe the complex structure of turbulent flow on the cellular scale at which blood damage is initiated.

Direct Lagrangian particle tracking provides an effective method for simulating micro-aerosol deposition in the upper respiratory airways. However, Xi and Longest [1] have shown that errors occurred in the predicted deposition rates of smaller particles in comparison to measurements. Matida et al. [2] attributed a similar discrepancy to the assumption of isotropic turbulent fluctuations near the wall. Matida et al. [2] implemented a near-wall anisotropic turbulence model and reported significantly improved agreement with experimental data. Longest and Xi [3] investigated nanoparticle deposition in oral airway models and showed that a Lagrangian transport model with a user-defined near-wall interpolation (NWI) algorithm provided an effective approach to accurately predict deposition in comparison to available experimental results. It is proposed that implementing both an anisotropic turbulence model with a NWI routine may further improve agreement between numerical and experimental results. The objective of this study is to evaluate the effect both near-wall anisotropic and interpolation models on regional deposition values in the oral airway geometry. Comparisons will be made to available in vitro test results. Models considered will include (1) the anisotropic correction only, and (2) anisotropic and NWI routines.

Vascular disease is the primary cause of morbidity and mortality in diabetics. Diabetic vascular disease is disseminated and includes renal capillary hypertrophy, reduced wound repair, impaired angiogenesis, and rapid and excessive hyperplasia after endovascular intervention [1, 2]. No single biochemical aberration unifies the diffuse nature of diabetic vascular disease. Hyperglycemia has been implicated, and yet glucose effects persist long after restoration of euglycemia. It is possible that acute fluctuations in glucose concentration have prolonged cell and tissue effects.

Cavitation formed during the closure of mechanical heart valves (MHVs) can harm nearby blood cells and valve surfaces. In this study we focus on an approach to accurately measure cavitation energy in order to compare the effectiveness of replacement valves. Cavitation energy is difficult to measure acoustically because it is masked by other pressure fluctuations in the body or system. To improve upon currently used analytical techniques, a wavelet isolation technique was developed to quantify cavitation energy. With this method, acoustic signals captured by a hydrophone are decomposed, denoised, and then reconstructed. Wavelet analysis should prove to be particularly valuable in vivo , where visual evidence of cavitation cannot be obtained.

Female athletes have significantly higher incidence of anterior cruciate ligament (ACL) injuries than males participating in similar sports [1]. To date, no clear explanation has emerged for this disparity. However, hormonal differences may provide an explanation because some ACL injuries have been linked to physiologic fluctuations in estrogen levels over the menstrual cycle [2]. Receptors for estrogen have been identified in rabbit and human ACLs and medial collateral ligaments (MCLs) [3]. Increased estrogen levels caused decreased fibroblast proliferation and collagen synthesis in cell cultures from human and rabbit ACLs [4]. Since fibroblasts maintain collagen production and degradation in ligaments and collagen is the major load-bearing component of ligaments, estrogen may affect knee ligament mechanical properties.

The optic nerve head (ONH) is the site of insult in glaucoma, the second leading cause of blindness worldwide. Intraocular pressure (IOP) is commonly regarded as a major factor in the onset and progression of the disease 1 and lowering IOP is the only clinical treatment that has been shown to retard the onset and progression of glaucoma 2 . However, many patients continue to progress even at an epidemiologically-determined normal level of IOP 3 . This suggests that in addition to the mean value of IOP, IOP fluctuations could be a factor in glaucomatous pathophysiology. The importance of low frequency fluctuations of clinically-measured mean IOP remains controversial. These studies all rely on snapshot measurements of mean IOP at each time point, and those measurements are taken at relatively infrequent intervals (hourly at the most frequent, but usually monthly or longer). Recently however, there has been some interest in ocular pulse amplitude, or the fluctuation in IOP associated with the cardiac cycle, which can be measured by Dynamic Contour Tonometry (DCT). DCT provides continuous measurement of IOP, but only for a period of tens of seconds in which a patient can tolerate corneal contact without blinking or eye movement, which ironically are two of the most common sources of large high frequency IOP fluctuations according to our telemetric data collected from monkeys 4 and previous human studies. In a recent report, continuous IOP telemetry was used in three nonhuman primates to characterize IOP dynamics at multiple time scales for multiple 24-hour periods 5 .

Fluid pressurization is the dominant load-bearing mechanism of the in vivo joint environment, supporting up to 90% of compressive loads in cartilage[1]. In accordance with its prominence in cartilaginous tissues, hydrostatic pressure (HP) significantly enhances the chondrogenic differentiation of mesenchymal stem cells (MSCs) [2,3]. However, surprisingly little is known about the mechanisms by which cells sense HP and translate it into a biochemical signal. This is partly due to the fact that HP generates a state of stress with little deformation, as hydrated tissues and cells are nearly incompressible. Because of this, it has been assumed that HP mechanotransduction differs from that of other mechanical loads which deform the cells [4]. Recently, we demonstrated that integrin binding to the pericellular matrix (PCM) regulates the cytoskeletal organization of MSCs, and this in turn determines their response to HP [5]. Another proposed mechanism of HP mechanotransduction is fluctuations in intracellular ion concentrations, which are altered by the application of HP [6–8]. In particular, calcium signaling has been implicated as a key regulator of cellular response in other mechanical loading modalities, yet no studies have examined the role of calcium in the response of MSCs to HP. Therefore the objective of this study was to examine the cellular proliferation and chondrogenic matrix accumulation of MSCs in response to HP in the presence of pharmacological inhibitors of calcium ion mobility in order to elucidate the role of calcium signaling in the mechanotransduction of HP.

Properly developed large elastic arteries serve as reservoirs that store stroke volume during systole and damp downstream blood pressure fluctuations. This function is enabled by the extracellular matrix (ECM) protein elastin. Mouse gene expression data reveals that elastin expression begins during embryonic development and peaks around postnatal day (P) 14. Expression then decreases to low levels for the remainder of adult life, indicating that elastin production during development is critical for a properly functioning vessel [1]. Reduced elastin in humans due to genetic mutations is associated with a congenital narrowing of the ascending aorta, known as supravalvular aortic stenosis, and chronic hypertension [2].

Low and/or oscillatory Wall Shear Stress (WSS) has been correlated with elevated risk for increased intima media thickness and atherosclerosis in several studies during the last decades [1, 2]. Most of the studies have addressed laminar flows, in which the oscillations mainly are due to the pulsating nature of blood flow. Turbulent flows however show significant spatial and temporal fluctuations although the mean flow is steady.

In this paper we simulate the effect of hydrodynamic interaction on the Brownian dynamics of semiflexible filaments. Semiflexible filaments are those whose entropy-driven bending fluctuations are resisted by the elastic bending stiffness. Semiflexible filaments make up the structural scaffold of cell and tissue matrix, and understanding their dynamic behavior is necessary for studying force transmission and remodeling in cells and tissue matrix. Hydrodynamic interaction refers to force on filament mediated through the local solvent flow around it. The local solvent flow is induced by the motion of the filament itself. Dynamic studies of semiflexible filaments tend to assume a uniform friction coefficient at every point on the filament. However Lagamarsino et al [1] showed that even for a filament in uniform translation, most of the drag is localized at the filament ends, which increases the tendency of the filament to bend and rotate even under a uniform driving force. In this paper we explore how the combined effect of non-uniform friction coefficient due to hydrodynamic screening and the non-uniform local solvent flow due to the filament fluctuations affects its Brownian dynamics.

When blood is pumped through the aortic valves, it has a time dependent flow with a relatively high speed, resulting in Reynolds numbers between 1500 and 3000. Hence, flow is in the transitional regime between laminar and turbulent flow. Transitional flow contains small scale fluctuations, see Figure 1, and may result in local high deformation rates.

As length scales decrease to microns, the mechanism for swimming becomes unfortunately counter-intuitive. In the macro-world, where human intuition has developed, we swim by accelerating the liquid around us. For microorganisms, which swim at Reynolds numbers much less than unity, Stokes law does not permit accelerations. As such, the fluid movement is governed entirely by the local boundaries of the microorganism and the fluid viscosity dampens velocity fluctuations rapidly as distance away from the swimmer increases. A well known byproduct of this, Purcell’s “Scallop Theorem”, forbids reciprocal motions to generate net forward movement [1]. To overcome this, flagella propagate waves down their length and cilia have asymmetric beats. This type of motility has been described as zero-thrust swimming since the net force on the organism-fluid system must be zero [2].

A balance board is an unstable platform which is currently used for training and rehabilitation to stabilize an individual’s upright posture. Models that examine how individuals remain upright while standing on an unstable surface are therefore needed to understand the mechanisms behind balance improvements. Most research in this area has focused on the fluctuations in posture about a static upright equilibrium using single-degree-of-freedom (1-DOF) inverted pendulum models [1–2]. While conceptually simple, these models nonetheless capture the stochastic, nonlinear and multiple timescale behavior of the fluctuations that are known to occur in human posture [1–3].

It has been previously reported in the literature that high-frequency diastolic heart murmurs in the myocardium occur in patients with coronary artery stenoses. It has also long been hypothesized that these murmurs are caused by flow instabilities downstream of the stenosis; the most obvious mechanism for this phenomenon is that pressure fluctuations due to the flow transition excite vibrations in the coronary artery wall which then radiate into the myocardium. A prior pilot study [1], utilizing Doppler vibrometry, an ultrasound based technique, was able to measure high frequency (100–1000Hz) but low amplitude (1–10 μm ) left ventricular wall vibrations in patients with coronary artery stenosis. Furthermore, the intensity of the wall vibrations was shown to significantly correlate with the percent stenosis (as determined by quantitative coronary angiography). This evidence suggests that ultrasound doppler vibrometry offers the possibility to detect coronary artery stenosis with a low-cost, relatively cheap, and non-invasive modality [2]. This particular study, therefore, seeks to quantify the relationship between the poststenotic flow instabilities and wall vibrations in order to optimize the vibrometry measurements.

Haematopoietic stem cells (HSCs) circulate in the bloodstream under flow conditions, but the mechanical mechanisms of governing their physiological trafficking in mammals are still not yet clearly understood. The mobilization of HSCs and their progenitors into the circulation represents the basis for modern bone marrow transplantation procedures [1]. Recently, Mendez-Ferrer et al. performed experimental investigations on mice [2]. They demonstrated that the circulating HSCs and their progenitors exhibit robust circadian oscillations, and the circadian fluctuations could also be significantly altered when the HSCs were subjected to different time of lighting. These results indicated that the photic cues could affect the trafficking of HSCs in healthy animals. This implies that the light is the stimulus of HSCs release. When the HSCs are exposed to light, the HSCs release would markedly increase; when the HSCs are in darkness, the HSCs release keeps low efficiency. In this study, we numerically simulate this phenomenon to study the mechanical mechanism of circadian fluctuations regulated HSCs release under the influence of periodic lighting time.

Fingertip forces during simple and static tripod grasp exhibit a surprisingly rich dynamics [1]. Here we explore the hypothesis that, even for this apparently simple manipulation task, these fluctuations are shaped by a neural controller rather than by signal-dependent motor noise. We fed band-limited noise processes scaled to mean force level into a 21-muscle model of 3-finger grasp, and compare model output with experimental force recordings. We find that the spatial and spectral characteristics of simulated force fluctuations differed greatly from those observed in actual static tripod grasp. In light of current literature [2], we propose that a continually active neural controller is at work even for this simplest example of multifinger manipulation.

Experimental studies of an impingement area inside aneurysms showed that loss of smooth muscle cells and degenerative remodeling of vessel walls occur at the region of high wall shear stress (WSS) and WSS gradient where the flow accelerates [1]. Also, a more sensitive response of endothelial cells to turbulent oscillatory shear rather than to laminar and steady shear has been demonstrated experimentally [2]. Therefore, it seems imperative to understand the spatio-temporal behavior of WSS vectors in the impingement (stagnation) locations. To this end, we investigate systematically the oscillatory behavior of WSS vectors inside aneurysms and the flow instability due to the presence of an aneurysm in the internal carotid arteries (ICA), more specifically, at the posterior communicating artery (PCoA) origin.