Annals of Biomedical Engineering

Background: Articulated laparoscopic instruments require a reliable mechanical connection between the handle and shaft to maintain the intended instrument configuration during surgical manipulation. The handle shaft locking interface should resist unintended relative displacement under external loading. However, the appropriateness of a specific slip resistance threshold must be evaluated in relation to the instrument design and intended conditions of use. Objective: To evaluate the mechanical performance associated with an 8 N slip resistance specification for the locked handle shaft interface of an articulated laparoscopic instrument using a controlled bench model. Methods: A bench based mechanical evaluation method was designed using the instrument under test, mechanical fixtures, a calibrated force measurement device, and displacement measurement equipment. After engagement of the handle shaft locking mechanism, external forces were applied to evaluate resistance to relative displacement. Testing included axial loading, loading in relevant transverse directions, and repeated locking unlocking cycles. The primary outcome was the force corresponding to the onset of relative slippage at the locked interface. Secondary outcomes included displacement under load, complete locking failure, and changes in mechanical performance after repeated operation. Acceptance criteria should be established before confirmatory testing. Results: All 30 instruments from three production batches met the 8 N axial requirement (30/30). The axial slip onset force was 12.40 N . Under a sustained load of 8 N for 60 s, mean relative displacement increased from 0.06 mm to 0.10 mm, and mean residual displacement was 0.02 mm. After 1,000 cycles, the axial slip-onset force was 12.00 N . Conclusions: This study provides a bench-testing framework for evaluating an 8 N slip resistance specification for the handle shaft locking interface of an articulated laparoscopic instrument. Whether this specification provides adequate mechanical stability can be determined only by comparing the measured performance with engineering acceptance criteria established in advance on the basis of the instrument's intended use and foreseeable loading conditions.

Introduction: The femoropopliteal artery undergoes substantial axial compression, bending, torsion, and pinching during limb flexion. When an implanted stent does not accommodate these deformations, repetitive biomechanical mismatch may alter the vascular response to implantation and contribute to restenosis. We tested whether designing a peripheral stent to better accommodate physiologic limb-flexion deformation reduces the subsequent inflammatory and neointimal response. Methods: A nitinol stent was developed using multi-objective computational optimization to maintain arterial apposition while reducing wall stress and luminal pinching during physiologic deformation. Sixteen Yucatan minipigs were studied in independent 3- and 6-month cohorts (n=8 each). Each animal received the optimized stent in one limb and a commercial stent with representative biomechanical behavior contralaterally. CTA quantified in vivo limb-flexion deformation, while CT and histology assessed stenosis, neointimal accumulation, inflammatory-cell burden, SMA-positive tissue, and extracellular-matrix composition. Results: The optimized stent accommodated greater axial shortening than the commercial comparator at both 3 months (11.2{+/-}2.7% vs. 6.6{+/-}2.1%, p=0.003) and 6 months (13.7{+/-}4.4% vs. 6.8{+/-}2.3%, p=0.004). Intimal hyperplasia volume was lower with the optimized stent at 3 months (227.5{+/-}85.2 vs. 350.0{+/-}130.5 mm3, p=0.002) and 6 months (183.6{+/-}46.2 vs. 261.2{+/-}60.6 mm3, p=0.001), with significantly lower maximum, mean, and median stenosis at both timepoints. At 3 months, macrophage and total inflammatory-cell counts were 51% and 45% lower, respectively, with the optimized stent. Histologic tissue area was 28% lower at 3 months and 12% lower at 6 months. SMA-positive tissue fraction was higher with the optimized stent at both timepoints, whereas elastin, glycosaminoglycan, and collagen fractions were similar between devices. Discussion: Improved accommodation of limb-flexion deformation was associated with a smaller inflammatory and neointimal response to stent implantation through 6 months, while overall neointimal matrix composition remained largely unchanged. These findings provide in vivo evidence that biomechanical compatibility with the dynamic lower-limb environment can influence vascular healing and should be considered a mechanistic design criterion for peripheral artery stents.

Healing of the gastrointestinal (GI) tract following surgical interventions is governed by coupled mechanobiological processes and may lead to severe complications such as perforation or stricture formation. A first comprehensive mechanobiological modeling framework of GI healing is herein proposed. The framework addresses two clinically relevant applications of bioprinting: endoscopic treatment of GI tissue defects and bioprinting-assisted surgical anastomosis. Tissue remodeling is based upon a hyperelastic material model with fiber dispersion coupling the spatiotemporal reaction diffusion dynamics of fibroblasts and cytokines with collagen deposition, reorientation, and plastic deformation. An active stress formulation drives fibroblasts and myofibroblast contraction while a multiplicative decomposition approach is adopted for collagen remodeling as a permanent change. The governing equations are discretised in time with an implicit Euler scheme, finite element in space and solved by a staggered algorithm implemented in the open-source platform FEniCS. Numerical simulations show that the initial collagen fibers content and orientation strongly influence fibroblast infiltration and scar contracture formation. The study quantifies the advantage of having a collagen bioprinted architecture aligned with tissue fibers, to reduce structural remodeling distortion. The model also predicts a strong correlation between collagen deposition and luminal burst pressure during the recovery of mechanical integrity in GI anastomosis.

The human pancreas secretes digestive fluid that flows through an extensive ductal network before emptying into the duodenum. However, little is known about how hydrodynamic forces influence pancreatic function and development. We hypothesized that pancreatic cells respond to physiological levels of fluid shear stress. In this study, we developed a microfluidic system featuring reversible sealing between the device layer and the cell culture substrate, enabling (1) conventional open-well cell culture prior to fluid shear stress application and (2) selective patterning of proteins and cells for migration studies. Channel dimensions were chosen to support 24-hour perfusion using standard syringe pumps. Using this platform, we investigated effects of physiological shear stress levels representing basal and activated pancreatic function (2, 8 and 33 mPa) on human iPSC-derived pancreatic progenitor cells. Pancreatic progenitor cells exhibit graded sensitivity to shear stress at the transcriptomic level. Specifically, shear stress upregulated expression of cell cycle-related gene sets; endocrine-associated genes including NEUROG3; and Notch receptor ligands (DLL1, DLL3) in a magnitude-dependent manner. The exposure to unidirectional fluid flow also resulted in a reduction in YAP1 protein content, decreased WWTR1 gene expression, and downregulation of YAP/TAZ target genes. Furthermore, barrier-based migration assays under shear stress revealed that cell patches expanded their boundaries both along and against the flow, with greater distance in the direction of flow. Our system and findings may help lay the foundation for understanding biophysical regulation of developmental processes in a physiologically important, yet hard-to-access, epithelial model system.

Tissue expansion is an established technique for the reconstruction of skin defects, but the cost of conventional silicone expanders may limit its application in contexts with lower resource availability. This study evaluated, in an experimental model, whether a container for storing saline solution could act as a low-cost alternative device for tissue expansion. An experimental, prospective, controlled and randomized study was carried out with 10 Wistar rats, distributed in two groups: conventional silicone expander and saline storage container. Both underwent the same surgical and expansion protocol. Abdominal circumference gain, final expanded skin length, histological and histomorphometric aspects of the skin, including collagen types I and III, as well as exploratory cost analysis, were analyzed. The conventional expander produced a greater gain in abdominal circumference, but the final length of the expanded skin was similar between the groups. Microscopic evaluation showed preservation of the cutaneous architecture, intact epidermis, cellularized dermis, and collagen deposition in both groups. There was no significant difference in the proportion of type I or type III collagen. The saline solution container had a substantially lower cost per centimeter of expanded skin than the conventional expander. These findings suggest that the saline container can produce experimental skin expansion with final length and collagen composition similar to the conventional method, at a lower cost, although additional studies are needed before clinical application.

Purpose: Atrial fibrosis is associated with thromboembolic risk in atrial fibrillation, but how fibrosis-related contractile impairment alters blood transport in the left atrium (LA) and left atrial appendage (LAA) remains unclear. Prior multi-physics simulations coupled electromechanical (EM) and computational fluid dynamics (CFD) models to show that fibrosis impairs LA function and flow, but were limited to booster-only contraction and could not separate the effects of fibrosis burden from its spatial distribution. Here we examined how fibrosis burden and spatial pattern independently relate to long-term LA and LAA hemodynamics in full-cycle, multi-beat simulations on a common LA anatomy. Methods: Three fibrosis patterns derived from late gadolinium enhancement MRI were considered: one from the patient providing the common anatomy and two from additional patients, with the latter mapped onto the common anatomy via universal atrial coordinates. All three patterns were applied globally at matched burdens of 15.6% and 31.2%, yielding six global-fibrosis cases and a non-fibrotic reference. Two patterns were also confined to the LAA at three local burdens (10%, 25%, and 50%), yielding six LAA-fibrosis cases. A 3D EM model for the LA anatomy was coupled to a 0D circulatory model, so that the simulations resolved the reservoir, conduit, and booster phases. Full-cycle EM-derived wall motion drove subsequent multi-beat CFD simulations. Region-specific emptying fraction (EF), non-dimensional kinetic energy (KE), and the 90th percentile of blood residence time (TR) were evaluated for the LA and LAA. Results: Left ventricular stroke volume remained nearly constant across cases, while increasing global fibrosis burden progressively reduced LA and LAA EF (LA: 36% to 30-31%; LAA: 44% to 28-38%) and monotonically increased LA TR across all patterns. Non-dimensional LA KE showed an approximately quadratic association with LA EF across patterns, whereas LAA KE was more scattered but still increased with LAA EF. In contrast, the relationship between the 90th percentile of LAA TR and LAA EF showed pattern-specific, non-monotonic trends. Conclusions: Fibrosis burden and spatial distribution jointly shape LA and LAA hemodynamics, but through different mechanisms. LAA EF is a robust functional descriptor of chamber-averaged kinetic energy regardless of fibrosis pattern, whereas LAA blood stasis depends additionally on the spatial distribution of fibrosis beyond what bulk emptying fraction predicts. These findings support incorporating imaging-derived fibrosis pattern, and not only burden, alongside functional metrics when assessing thrombogenic risk in the LAA.

Vector flow mapping (VFM) reconstructs left-ventricular (LV) blood velocity from color-Doppler echocardiography by combining the measured beamwise component with physical and regularizing constraints. Analysis of the discrete VFM formulation shows that the inverse problem is intrinsically ill posed: the occurrence of singular modes can be predicted from the geometry of the segmented blood-pool domain, the imposed boundary conditions, and the degree of smoothing. These modes can propagate uncertainty along entire transverse bands of the reconstructed velocity field, yet conventional VFM neither quantifies this uncertainty nor allows for correcting the blood-pool segmentation. We introduce Bayesian VFM (B--VFM), a hierarchical framework that jointly infers radial and transverse velocities, a probabilistic blood-pool mask, their spatially resolved uncertainties, and hyperparameters weighting Doppler and segmentation fidelity, mass conservation, boundary conditions, and smoothness. The discretized posterior admits a closed-form gradient and exact Hessian, enabling computationally efficient, gradient-based MAP estimation, sampling, and direct analysis of ill-posed modes. Posterior inference combines Gibbs sampling of conjugate Gamma-distributed hyperparameters with conditional maximum-a-posteriori estimation and a Laplace approximation for the high-dimensional velocity and mask fields. To accommodate systematic departures from planar mass conservation, B-VFM can learn the covariance of the planar divergence residual from an ensemble of flows and incorporate it as a structured model-discrepancy prior. Independent chains converged reproducibly, while covariance priors learned from flow ensembles illustrated how model discrepancies can be incorporated into the inference. B--VFM was evaluated using Lamb-Chaplygin dipoles under ideal conditions and with Doppler corruption, Doppler voids, and segmentation defects, and using the Hicks-Moffatt family of spherical vortices to assess violations of planar mass conservation. The method produced smooth reconstructions, localized uncertainty near unreliable measurements and regions of model inconsistency, and used flow information to correct segmentation errors. Within the tested vortex family, the data-informed planar divergence prior reduced velocity bias and mask distortion. B--VFM thus provides an uncertainty-aware reconstruction method and a flexible foundation for future VFM formulations incorporating additional priors, observations, and physical models. Future work will evaluate the method using clinical data and more complex three-dimensional benchmark flows.

Seroma is a common complication following abdominoplasty and other procedures involving extensive soft tissue dissection. Although animal seroma models have been reported, the stromal pathology underlying post-abdominoplasty seroma, particularly the role of oxidative stress, remains poorly characterized. Here, we developed a rat abdominal seroma model by surgically separating the subcutaneous tissue from the underlying muscle fascia and investigated the temporal evolution of the associated stromal response. Seroma developed in 9 of 20 operated rats, corresponding to a formation rate of 45.0%. Longitudinal ultrasound demonstrated that fluid accumulation peaked around postoperative day (POD) 7 and largely resolved by POD30. Despite macroscopic fluid resolution, substantial stromal remodeling persisted. Compared with normal abdominal tissue, seroma-associated tissues at POD14 and POD35 exhibited increased collagen deposition, macrophage accumulation, oxidative injury, and vascular remodeling. Additionally, at POD35, macrophage accumulation and 4-hydroxynonenal staining were greater than at POD14, whereas collagen deposition and vascular density remained elevated with no significant differences between postoperative time points. To our knowledge, this study presents the first rat model specifically designed to reproduce post-abdominoplasty seroma and the first temporal characterization of oxidative stress within seroma-associated tissue. These findings reveal that seroma fluid resolution does not coincide with stromal recovery and identify persistent oxidative stress, inflammation, fibrosis, and vascular remodeling as important features of seroma pathology.

Predictive biomechanical models of the tricuspid valve require accurate representation of the chordae tendineae, yet subject-specific chordal geometry is difficult to reconstruct from non-invasive imaging. Here, we adopt a framework for generating functionally equivalent synthetic chordae without prior knowledge of in vivo chordal attachments. To this end, we first adapt an anatomy-informed hyperelastic shape-matching method that establishes correspondence between end-diastolic and end-systolic leaflet configurations using chordal-mimicking forces, a rigid contact template, and a Gaussian-smoothed locally corrective pressure field. We then generate synthetic chordal insertion sites using zone-based rejection sampling and calibrate the unloaded length of each chord by combining reaction forces with the chordal stress-stretch relationship. The framework was evaluated using Texas TriValve 1.1, a high-fidelity finite element model of a human tricuspid valve validated against beating-heart echocardiography. We found that shape matching reproduced the target end-systolic geometry with a mean inter-surface distance of 0.29 {+/-} 0.35 mm. Moreover, synthetic chordal insertions faithfully reproduce end-systolic leaflet deformations. We subsequently examined synthetic chordal configurations containing 202, 225, and 450 insertions, informed by measurements from eight explanted human tricuspid valves. Here, increasing insertion number reduced mean inter-surface distance from 0.63 {+/-} 0.52 mm to 0.49 {+/-} 0.44 mm and reduced contact area errors from 3.52% to 0.59%. Across all configurations, mean maximum principal stretch errors in leaflet belly regions remained below 2.4%, while areal strain errors ranged from 0.34% to 10.01%. These results demonstrate that anatomically informed shape matching coupled with stress-based chordal calibration can reproduce tricuspid valve closure without explicit subject-specific chordal geometry. This framework provides a foundation for generating synthetic subvalvular anatomy for future imaging-derived, predictive tricuspid valve models.

Background: Hypertension is a major risk factor for type B aortic dissections and rupture, with guidelines recommending systolic blood pressure (SBP) control below 130 mmHg to improve outcomes. While post-TEVAR blood pressure is often managed with a focus on mean SBP, little is known about temporal hemodynamic patterns and their association with surgical success. This study investigates blood pressure and heart rate (HR) time-series metrics within 24 hours post-TEVAR and their predictive potential for outcomes. Methods: Blood pressure (n = 560) and HR (n = 680) time-series data from 31 patients were analyzed alongside preoperative aortic geometry metrics. Exploratory data analysis identified correlations between BP variability and outcomes. Stationarity tests were performed on time-series data to assess statistical properties. Logistic regression models incorporating hemodynamic metrics, along with CT-derived features, were used to predict TEVAR outcomes. Results: Successful outcomes correlated with greater diastolic blood pressure variability and strictly stationary SBP. Logistic regression models combining these metrics along with heart rate standard deviation and preoperative aortic geometry achieved 96.67% 5-fold cross-validation accuracy in predicting outcomes. Conclusion: Post-TEVAR behaviors of hemodynamic variables are critical predictors of TEVAR success, with higher DBP standard deviation and strict stationarity of SBP significantly associated with favorable outcomes. These findings highlight the importance of hemodynamic variability and stationarity in optimizing post-TEVAR patient care.

Point-of-care (POC) molecular detection has enabled rapid and accessible testing at or near the site of need, facilitating timely decision-making in clinical, field, and industrial settings. Despite these advancements, molecular detection platforms remain limited in their ability to prepare DNA from complex tissue matrices, restricting their applicability to a narrow range of sample types. To address sample preparation inefficiencies, focused ultrasound extraction (FUSE) has been developed for the rapid release of DNA from robust tissue matrices. FUSE disintegrates target tissue and releases DNA by delivering high pressure ultrasound pulses that generate a cavitation bubble cloud. In prior work, FUSE was performed using large, laboratory-based equipment. Here, a miniaturized FUSE device was designed and tested to enable POC DNA sample preparation. Design constraints were defined based on prior FUSE experiments, and based on these metrics, a 750 kHz cylindrical transducer was fabricated. The pressure output was measured, and high-speed optical imaging demonstrated that the transducer generated sustained cavitation within the defined focal region. The feasibility of DNA extraction from piscine and timber tissues was evaluated, and results show that the device can release DNA with quality suitable for PCR-based detection from both tissue types. These results demonstrate the potential of this device to rapidly extract DNA from complex samples and expand the applicability of molecular detection platforms.

Devireddy et al. [1] previously showed that an enthalpy-based, macroscale model simulated tissue freezing histories are in close agreement with a coupled model incorporating cellular water transport and intracellular ice formation (IIF). That comparison, however, was performed for a limited set of tissue geometries, cooling conditions, and biophysical parameters. Here, we revisit that conclusion by reimplementing the published model from its governing equations and systematically expanding the parameter space to determine when microscale processes alter the predicted macroscale freezing response. We incorporate both surface catalyzed nucleation (SCN) and volume catalyzed nucleation (VCN) of intracellular ice with cellular osmotic dehydration and examine a broad range of tissue dimensions, cooling rates, convective boundary conditions, membrane permeabilities, cell sizes, activation energies, intracellular water fractions, and nucleation rates. Linearization of the cellular water transport equation about osmotic equilibrium yields an osmotic relaxation timethat can be compared with the local residence time of tissue undergoing phase change. Their ratio defines a dimensionless group, that organizes the transition between regimes in which the uncoupled enthalpy formulation and the coupled micro and macroscale formulation produce similar or substantially different results. Across the one-dimensional parameter space examined here, the two models remain within a prescribed thermal-error bound for the dimensionless group below approximately 0.1, whereas the discrepancy increases systematically above this threshold. Model divergence also depends on intracellular ice nucleation, i.e., when nucleation is sufficiently slow, cellular water transport can become rate limiting for latent heat release. Conversely, sufficiently rapid intracellular ice formation reduces the macroscopic discrepancy by providing an additional pathway for latent-heat release. Multidimensional simulations further show that geometry alone can move a nominally conventional freezing protocol into the coupled regime. In particular, multidirectional cooling can reduce the local residence time sufficiently to produce substantial differences in predicted frozen volume even when the corresponding thermal histories appear similar. Finally, we formulate an inverse approach for estimating IIF parameters from tissue scale thermal histories. Synthetic simulations indicate that parameter recovery is feasible within a finite range of cooling conditions, providing a testable strategy for future experimental measurements. Together, these results provide a mechanistic criterion for deciding when microscale biophysical processes must be retained in macroscale tissue-freezing models.

A densely vascularized tissue can still be starved of oxygen. Tissue oxygenation depends heavily on vessel arrangement, blood flow distributions, and cellular metabolism. Resolving these effects from individual constituent vessels to whole organs has historically been computationally prohibitive. We introduce the Cardiovascular Analysis and Simulation of Circulatory Advection, Diffusion, and Exchange (CASCADE) toolkit, which makes vessel-resolved oxygen transport tractable at the organ scale through a novel screened Green's-function formulation. On laptop-class hardware, CASCADE simulates networks containing thousands of vessels in under one second and a full biventricular human heart model in about two minutes. We validate spatial oxygen and cell-survival predictions against experiments in perfused engineered tissues and matched finite-element simulations. In engineered tissues, sweeps across thousands of network designs and physiological conditions reveal when vessel density, oxygen supply, or network architecture limits viability, establishing design rules for sustaining thick constructs. In a human heart model, CASCADE translates coronary occlusion, anemia, polycythemia, and hypoxemia into distinct myocardial oxygenation patterns, revealing where oxygen delivery fails and how much tissue is at risk.

Marker-based optical motion capture remains the gold standard for kinematic analysis across biomechanical research. However, when tracking dynamic movements, severe occlusions often create missing data and noisy signals that require time-consuming manual cleaning. Existing automated methods usually rely on predefined skeleton models or need massive training datasets for machine learning solutions. This study presents the AMP: an automated marker based motion capture processing pipeline. The AMP is a fully analytical approach that uses hierarchical algorithms including 1) rigid-body constraint, 2) Kalman Filter state estimation and 3) kinematic pattern match to label markers and fill data gaps without manual human intervention. First, the algorithm identifies and removes mislabeling markers before any data scrubbing. During the data cleaning process, our hierarchical algorithm uses a translation-based step to track segments even when there are insufficient donor markers to form a full rigid body. To reconstruct missing marker trajectories, the pipeline initially uses Piecewise Cubic Hermite Interpolating Polynomial (PCHIP) interpolation for short marker gaps. However, the PCHIP creates massive spatial errors during long occlusions, the system automatically switches to rigid-body tracking for gaps over 40 ms. Results showed the pipeline drastically reduced processing time compared to manual human expert methods by 73.5%. In addition, the AMP kept spatial errors within 10 mm of the manual ground truth. By using this combined hierarchical approach to match marker processing accuracy, the pipeline provides a fast, general-purpose tool that fully automates data cleaning and saves hours of manual effort.

Purpose: To quantify, in a computational fluid dynamics (CFD) benchmark, how spatial degradation, temporal acquisition and noise change the error of plane-based pulmonary-artery flow endpoints. Methods: Twenty-two historical, non-converged CFD simulations (11 geometry families) were voxelised at 2 mm with 80 frames per cycle. Simulations with numerical divergence were excluded, leaving 13 (7 families). Fields were degraded to 4 and 8 mm and with noise, plane waveforms were sampled at 20 phases with one-interval averaging, and errors were computed against the noise-free reference waveform on 66 geometric planes. Family-mean paired differences are reported with t-based 95% confidence intervals under an analysis plan fixed in advance. Results: Spatial degradation from 2 to 4 mm increased full-waveform nRMSE by 0.0032 [0.0021, 0.0043], in 7 of 7 families; cycle-mean flow bias accounted for 23% of the squared error, against 60% at 8 mm. With SNR scaled to voxel volume, the increase was not resolved (0.0002 [-0.0012, 0.0015]). Twenty-phase acquisition increased PI error (0.0223 [0.0214, 0.0233]) and diastolic-trough timing error (0.63 [0.52, 0.74] frames) more than spatial degradation, and its point estimates for these endpoints were larger with every recovery method; the nRMSE ordering and peak timing depended on the recovery method. The implementation of the downsampling operator mattered: an alternative, corner-aligned implementation of the same 4 mm degradation gave a larger spatial effect (nRMSE difference 0.0010 [0.0002, 0.0017]). Conclusion: In this benchmark, a 2 to 4 mm degradation produced a small, consistent, mostly shape-related nRMSE increase that depended on the noise model, whereas 20-phase acquisition changed PI error and trough timing more. The results describe benchmark behaviour, not clinical acquisition requirements.

Conventional clinical assessment of upper limb kinematics relies on goniometry or visual estimation, methods that provide limited information on multi-segment 3D kinematics and can have poor inter-rater reliability. Inertial measurement units (IMUs) represent a viable alternative; however, extracting anatomically meaningful joint angles from skin-mounted sensors remains challenging owing to sensor-to-segment misalignment, soft-tissue artefact, and suboptimal orientation estimation under dynamic conditions. This study developed and validated a multi-segment IMU-based framework for upper limb kinematic assessment, addressing three stages of the measurement pipeline: (i) sensor fusion gain optimisation as a function of task mean segment angular velocity; (ii) accuracy of an anatomical landmark registration-based alignment method; and (iii) comparative evaluation of landmark-based alignment against manual and neutral-pose alignment approaches. Twenty participants with typical shoulder function performed clinical and functional upper limb tasks, recorded simultaneously with an optoelectronic motion capture system and six IMUs tracking the thorax, clavicle, scapula, humerus, forearm, and hand. Orientation estimation used a gradient-descent complementary filter with velocity-dependent gain modulation. Sensor-to-segment alignment was achieved via manual, neutral-pose, and landmark registration methods. Mean sensor orientation errors ranged from 1.5 to 3 degrees across segments/tasks and increased with angular velocity. Landmark registration produced substantially lower joint angle errors than manual and neutral-pose alignment across all joints (root mean square error range: 3.7-7.8 degrees; manual: 8.3-24.2 degrees; neutral: 15.5-35.5 degrees). These results indicate that IMU-derived kinematic accuracy is context-dependent, varying with joint and movement type, suggesting that accuracy should be established for the specific movements and joints relevant to each clinical application.

Patients with implantable cardioverter-defibrillators (ICDs) often are excluded from receiving CMR scans at 3.0T due to ICD-induced image artifacts. This work aims to transfer sequence protocols established for CMR imaging in the presence of ICDs at 1.5T to a first human application at 3.0T. All measurements were performed on a clinical 3T MRI scanner. Phantom measurements were used to establish and optimize wideband PSIR LGE imaging at 3.0T. Volunteer measurements with externally placed ICDs were used for optimization of CINE imaging and wideband PSIR imaging. Thirdly, patients with implanted ICD were examined with the optimized protocols. Human measurements showed that SA stacks obtained with spoiled GRE after contrast agent showed a markedly lower artifact burden than the conventional approach. For scar imaging, a wideband PSIR with a bandwidth of 3kHz and a frequency offset of +750Hz allowed a sufficient suppression of relevant artifacts in the majority of scans. No strong correlation between the image quality and the distance between the cardiac silhouette and the device was detected. The presented work shows the feasibility of clinical cardiac MRI at 3.0T including GRE-CINE and wideband PSIR-LGE for patients with ICDs.

Fibrotic strictures are among the most disabling complications of Crohn's disease, permanently narrowing the bowel and impairing motility, yet no approved therapy reverses them. Chronic inflammation alters pacemaker-network coupling, smooth-muscle excitability, and calcium-dependent contractility, while fibrosis thickens the bowel wall, narrows the lumen, and changes tissue mechanics. The relative contributions of these coupled electrical, contractile, and structural alterations to motility loss remain unclear. To address this gap, we develop an integrated electromechanical finite-element framework for fibrostenosing Crohn's disease that couples a fibrosis-driven growth model with a FitzHugh-Nagumo electromechanical model. A full-factorial 25 design of experiments is used to quantify the relative effects of electrical diffusivity, excitation threshold, peak active stress, wall stiffness, and hypertrophic remodeling on cyclic lumen-volume deformation. Motility is quantified by the standard deviation of lumen volume over one contraction cycle. Within the parameter ranges examined, increased wall stiffness emerged as the dominant contributor to motility loss, followed by impaired smooth-muscle contractility. Changes in excitation threshold, hypertrophic remodeling, and electrical diffusivity produced substantially smaller effects. Pairwise interactions were small relative to the dominant main effects, indicating that the mechanisms contributed largely through their individual effects. Our findings suggest that limiting wall stiffening while preserving smooth-muscle contractile function may provide a therapeutic strategy for maintaining intestinal motility in fibrostenosing Crohn's disease.

The ability to generate vascularized tissue constructs supplied by surgically accessible vessels remains a major limitation in reconstructive tissue engineering. Previous work demonstrated that positioning porous biomaterials around a vein can induce extensive vascular sprouting and generate a vascularized tissue volume without creation of an arteriovenous loop. However, this phenomenon has principally been demonstrated using rigid calcium-phosphate scaffolds, limiting its direct relevance to soft-tissue reconstruction. Here, we investigated whether a flexible decellularized dermal matrix could similarly be vascularized around a single unmodified vein and whether autologous dermal fibroblasts could further enhance this response. Decellularized rat dermis, with or without autologous dermal fibroblast seeding, was implanted either subcutaneously in the dorsal region or around the femoral vein for 8 weeks. Following Microfil perfusion, three-dimensional micro-CT demonstrated an extensive branching vascular network within perivenous constructs. Vessel volume relative to tissue volume was 0.2 +/- 0.1% in subcutaneous constructs without fibroblasts (n = 11) and 0.6 +/- 0.2% with fibroblasts (n = 9), compared with 6.+/- 1.4 % in perivenous constructs without fibroblasts (n = 10) and 7.3+/- 1.2% with fibroblasts (n = 10). Histology and immunohistochemistry similarly showed greater cellular repopulation and substantially higher CD31- and -SMA-positive vessel densities following perivenous implantation. Integrated two-way ANOVA of the same 8-week data confirmed a dominant effect of implantation site across the vascular outcomes, while fibroblast seeding significantly affected vascular volume, dermal remodeling, and nuclear density. The effect of fibroblast seeding on vascular volume was site dependent, with a significant implantation site fibroblast interaction. At 8 weeks, the vascularized dermal construct was completely dissected free from the surrounding tissues while maintaining its connection to the femoral vein. A small superficial incision into the isolated dermis produced visible bleeding, supporting an acute functional connection of the intradermal vascular network to the host circulation while the femoral venous connection was preserved. After flap elevation, perivenous constructs retained substantially greater vascular volume and showed more complete surface healing and organized skin architecture than subcutaneous constructs. Fibroblast seeding accelerated wound closure, while its effect on post-elevation vascular volume depended on implantation site: VV/TV decreased in subcutaneous constructs but increased in perivenous constructs. These findings show that single-vein vascularization can extend from rigid calcium-phosphate biomaterials to a compliant biological extracellular-matrix scaffold and may provide a simplified axial vascularization strategy without arterialization or incorporation of an arterial vessel.

Objectives: To develop and validate pixel data analysis (PDA) for reconstructing pixel-level shear-wave velocity (SWV) from saved Holder-Optimized Elastography (HOE) elastograms and to determine whether whole-field subcutaneous heterogeneity provides a quantitative signature of lymphatic obstruction compared with visual high-velocity-area (HVA) counting and sparse manual region-of-interest (ROI) sampling. Materials and Methods: In this cross-sectional study, 110 women after breast cancer surgery underwent lymphoscintigraphy and HOE, a pressure-minimized acquisition framework that preserves conventionally captured SWV information while additionally revealing spatial abnormalities attenuated by handheld acquisition. Reconstruction validation used 200 paired ROIs from 49 PACS-retrieved images spanning nearly the full displayed SWV range; reproducibility was assessed across 96 matched anatomical sites from 6 participants undergoing independently reacquired HOE examinations. PDA, visual HVA counting, and manual ROI sampling were evaluated on the same HOE-acquired elastograms in task-specific common complete-case cohorts. Results: PDA reconstructed machine-reported SWV with near-zero error (mean difference, +0.0009 m/s; mean absolute error, 0.0075 m/s; 95% limits of agreement, -0.0202 to +0.0221 m/s). For subcutaneous variance, interobserver/intraobserver ICCs were 0.718/0.799 for PDA and 0.161/0.560 for manual ROI sampling. In the primary no-versus-partial comparison (n = 93), forearm-pooled PDA subcutaneous variance ratio yielded the highest observed AUC (0.859; 95% CI, 0.772 - 0.947), compared with 0.820 for visual HVA counting and 0.769 for manual ROI sampling. PDA's subcutaneous variance ratio remained a leading feature across all three comparisons (AUC, 0.859 - 0.878), including partial-versus-total grading, where all three frameworks showed high discrimination. Conclusions: PDA accurately reconstructs pixel-level SWV from saved HOE elastograms and enables reproducible whole-field quantification of superficial SWE heterogeneity. Subcutaneous variance ratio was the leading quantitative PDA feature across lymphatic-obstruction comparisons and was particularly informative in partial obstruction. The same approach also enables retrospective quantitative reanalysis of compatible archived elastograms.