Mechanical forces are increasingly recognized as potent regulators of inflammation. Physical cues such as stretch, tissue stiffness, and shear stress shape innate immune responses across barrier epithelia, stromal niches, and the vascular endothelium. By engaging conserved mechanotransduction pathways, these forces both modulate and initiate mechano-inflammatory programs, remodeling immune synapses, reconfiguring tissue architecture, and directing leukocyte trafficking. When tissue mechanics are chronically perturbed through sustained pressure, matrix remodeling, or disturbed flow, these same pathways drive pathological inflammation and contribute to diseases ranging from asthma and arthritis to fibrotic disorders and atherosclerosis. In this review, we position mechano-inflammation as a unifying framework linking physical forces to immune regulation. We also highlight diagnostic and therapeutic opportunities targeting the mechanical dimension of immunity.

To investigate the relationship between the contact site and fracture patterns under static loading using finite element analysis (FEA). Although temporal bone fractures often lead to critical otologic complications, such as hearing loss and facial palsy, their mechanisms are not well understood. Two types of cranial models were developed: a "Simplified model" (S-model) using geometric approximations, and a "Precise model" (P-model) reconstructed from head CT images of a 40-year-old male. Static structural analysis was performed, and static loads were applied to the vertex, left temporal, and occipital regions. First, fracture initiation was estimated from the first principal shear stress, and then fracture propagation paths were predicted from the distribution of the vectors for the first principal stress distribution. S and P-models showed similar stress distribution patterns with some differences; thus, we used the S-model for general mechanical analysis and P-model for anatomically detailed evaluation. Under some loadings, high-stress concentrations were observed at both the contact site and temporal squama. Temporal loading induced stress distributions roughly similar to longitudinal fractures along the petrous ridge. Occipital loading resulted in stress concentration around the foramen magnum, suggesting a correlation with transverse fracture patterns. As an initial simulation effort, the results partially reproduced the clinical correlation between contact site and fracture orientation (longitudinal vs. transverse) under static analysis conditions. This mechanical approach provides a theoretical basis for predicting internal injuries from external trauma. Future refinements incorporating dynamic loading and internal structures are necessary to enhance diagnostic accuracy in emergency situations.

The incorporation of side branches in vessel geometry influences wall shear stress (WSS) distribution. However, complete vessel reconstruction is time-consuming, and there is no evidence that its WSS estimations better predict atherosclerotic disease progression compared with the output of the conventional single-vessel reconstruction (SVR). Patients who had baseline and 1-year follow-up intravascular ultrasound imaging (n=40 vessels), and patients with neoatherosclerotic lesions (n=13 vessels) on optical coherence tomography were included. All the studied vessels had at least one side branch with a diameter >1 mm; 3-dimensional complete vessel reconstruction and SVR were performed, and the time-averaged WSS and multidirectional WSS were computed. The performance of both methods in predicting disease progression in intravascular ultrasound and optical coherence tomography models was assessed. The incorporation of side branches in 3-dimensional geometry resulted in lower minimum predominant time-averaged WSS in the intravascular ultrasound (1.09 versus 1.58 Pa, P<0.001) and optical coherence tomography-based reconstructions (0.68 versus 1.33 Pa, P<0.001) and influenced the multidirectional WSS distribution. In native segments, complete vessel reconstruction-derived WSS metrics demonstrated superior predictive performance for disease progression-defined as lumen area reduction and plaque burden increase-compared with SVR, as evidenced by improved out-of-sample accuracy (leave-one-out information criterion: 429 versus 551), discrimination (C statistic: 0.725 versus 0.651), calibration (Brier score: 0.172 versus 0.226), and explained variance (27.8% versus 20.7%). Consistent findings were observed in stented segments, where complete vessel reconstruction-derived WSS metrics more accurately predicted neointimal proliferation than SVR-derived metrics. Incorporating side branches into vessel reconstruction influences WSS distribution and enables more accurate prediction of atherosclerotic disease progression in native and stented segments than SVR.

The assumption that blood adheres to vessel walls with zero tangential velocity component, the so-called "no-slip" boundary condition, is a foundational premise of cardiovascular fluid dynamics. Whether the no-slip condition holds in vivo, however, remains unknown. Seven healthy adult volunteers underwent cardiovascular magnetic resonance imaging. With four-dimensional flow magnetic resonance imaging of the descending thoracic aorta and modeling blood as a Navier-Stokes fluid, near-wall blood velocities were quantified, and wall shear stress was calculated based on the measured velocity fields. Within the Navier-Stokes data assimilation framework, tangential wall velocities of ∼30-80% of the mean luminal velocity were consistently obtained. These results provide evidence for effective macroscopic slip behavior at the aortic wall in vivo. Consequently, wall shear stresses were substantially reduced compared with values obtained under the assumption of no-slip. This finding challenges the universal use of the classical no-slip boundary condition in macroscopic cardiovascular flow modeling and directly affects key blood flow characteristics such as pressure drop, vorticity, wall shear stress, and energy dissipation, which play important roles in both normal and disease-state cardiovascular conditions.NEW & NOTEWORTHY Using in vivo magnetic resonance imaging data from healthy adult volunteers, we provide evidence for effective macroscopic slip behavior along the endothelial surface in the descending thoracic aorta. Not a single case exhibited zero tangential velocity, which would define the classical no-slip boundary condition. We introduce a robust analysis framework that ensures consistent and reproducible results across manual, AI-based, and uniformly dilated AI-based vascular segmentations.

BackgroundArterial cannulation during cardiopulmonary bypass (CPB) significantly alters native aortic hemodynamics by generating a high-velocity jet that interacts with the ascending aorta and aortic arch geometry. These flow disturbances may influence wall shear stress (WSS), turbulence intensity, embolic trajectories, and cerebral perfusion. Cannula depth, orientation, and tip design have emerged as potentially important determinants of intra-aortic flow behavior.Materials and methodsA structured narrative review of the literature was conducted. PubMed/MEDLINE, Scopus, and Web of Science were searched from January 1990 to April 2025. Keywords included combinations of "aortic cannulation," "cardiopulmonary bypass," "computational fluid dynamics," "wall shear stress," "turbulence," "atherosclerotic plaque," "cerebral perfusion," "microembolization," "gaseous emboli," "NIRS," and "transcranial Doppler." Studies were included if they evaluated hemodynamic effects of cannulation strategies using computational, in vitro, or clinical models. Articles not directly related to CPB intra-aortic flow dynamics were excluded.ResultsThe available evidence suggests that cannula positioning significantly influences intra-aortic flow behavior. Centrally aligned cannulation directed toward the descending thoracic aorta promotes axial flow and is associated with reduced jet-wall impingement and lower peak WSS. This configuration decreases arch turbulence and limits embolic transport toward supra-aortic vessels.ConclusionArterial cannulation strategy during CPB is a modifiable determinant of flow behavior and potential cerebral embolic exposure. Hemodynamically informed cannulation principles may contribute to intraoperative neuroprotection, although prospective clinical validation is still required.

Geriatric patients with isolated systolic hypertension (ISH) and wide pulse pressure (PP) were treated using enhanced external counter pulsation (EECP) combined with amlodipine versus amlodipine alone. The efficacy of both treatment modalities was assessed based on hemodynamic parameters. Retrospectively included 132 elderly patients with ISH and wide PP in our hospital (Mar 2022-Jun 2024). After exclusion, 120 cases were analyzed and divided into the amlodipine group and the combined group. Primary indicators include endothelin-1 (ET-1), nitric oxide (NO), systolic blood pressure (SBP), PP, systemic vascular resistance (SVR), coronary flow reserve (CFR), flow-mediated vasodilatation (FMD); secondary measures include mean arterial pressure (MAP), wall shear stress (WSS) and adverse reaction incidence. After 4 courses of treatment, patients in the combined group had significantly lower rates of ET-1, SBP, PP, MAP, SVR and the incidence of adverse reactions (all P<0.05); NO, FMD, WSS and CFR were higher (all P<0.05) than in the amlodipine group. EECP plus amlodipine has advantages over amlodipine monotherapy in treating elderly patients with ISH and wide PP, which provides a scientific basis for optimizing clinical treatment.

Sickle cell anemia (SCA) is the most severe form of sickle cell disease and causes increased stroke risk, even in children. Hemodynamic mechanisms underlying cerebral vasculopathy remain unclear. To test the hypothesis that SCA causes disturbed flow and increased regions of low wall shear stress (WSS) in cerebral arteries, we combined high-frequency ultrasound, micro-computed tomography, and computational fluid dynamics (CFD) using mice that are homozygous sickle (SS) and heterozygous trait (AS) at 4, 12, and 24 wk of age. At 12 wk, common carotid artery diameters were 12.4%-18.6% larger in SS mice (P < 0.02), but common carotid inflow, blood velocity, and WSS did not differ significantly between genotypes. SS cerebral arteries demonstrated that branch- and age-specific reductions in velocities and volumetric flow were measured in SS cerebral arteries, particularly the middle cerebral artery (MCA), independent of common carotid artery inflow. Time-averaged mean-of-the-maximum velocity (TAMMV) was ∼40%-50% lower in the MCA of SS mice at 4 and 12 wk (P < 0.03), and MCA volumetric flow was lower by 56%-67% (P < 0.05). CFD models revealed more regions of low WSS (<5 dyn/cm2) in cerebral arteries of SS mice, even in straight regions of the arteries at 12 and 24 wk. Our findings indicate that SCA reduces blood velocity and volumetric blood flow in the cerebral arteries while increasing endothelial exposure to pathological shear stress, providing a link between altered hemodynamics and arterial wall damage unique to sickle cell disease.NEW & NOTEWORTHY Sickle cell disease hemodynamics identifies: 1) stenoses and aneurysms along the lengths of carotid and cerebral arteries in sickle cell transgenic mouse model; 2) disturbed flow in the straight regions of the carotid and cerebral arteries; and 3) reduced blood flow and increased regions of low wall shear stress can predispose cerebral arteries to pathological and accelerated arterial damage and risk of strokes.

AI‑guided design of 3D-printable gyroid spacers for scale‑resistant membrane distillation in sustainable water treatment.

Blood pumps generate non-physiological shear stress (NPSS) that activates platelets and disrupts haemostasis. Ticagrelor is used in antiplatelet therapy for mechanical circulatory support, yet its effects under NPSS remain unclear. This study investigated how ticagrelor and NPSS interact to modulate platelet haemostatic function. Citrated bovine blood was circulated in a Rotaflow loop (500 ml, 5.0 l·min-1, ΔP of 0, 100 and 350 mmHg) for up to 3 h. Ticagrelor (20 μM) was administered either before circulation or after shear stress exposure. Flow cytometry and aggregometry quantified platelet activation, P2Y12 receptor surface expression, adhesion and aggregation. Proteomics compared signalling across treatment sequences, and thromboelastography (TEG) assessed clot kinetics. NPSS increased P-selectin, GPIIb/IIIa expression and fibrinogen adhesion and reduced P2Y₁2 receptor surface expression. Ticagrelor suppressed adenosine diphosphate (ADP)-induced aggregation and attenuated shear-driven platelet activation and also mitigates shear-induced loss of platelet P2Y₁2 surface expression. Proteomics showed lower Gi-coupled signalling and relative preservation of cAMP-PKA-related proteins, with the post-ticagrelor group showing the strongest suppression of activation signalling. As the ΔP of loop increases, the drug's ability to inhibit activation decreases. TEG showed faster clot initiation and growth after shear exposure, and these changes were most effectively moderated when ticagrelor was administered after shear exposure. NPSS activates platelets through pathways linked to Gi signalling. Ticagrelor reduced shear-induced activation, with the greatest reduction when used after shear. These findings support timing as a controllable variable during blood pump support.

Arteriovenous (AV) fistulas, the preferred vascular access for hemodialysis, fail to mature in up to 60% of patients with kidney failure. This high failure rate is often attributed to adverse hemodynamic conditions, yet the exact mechanisms remain poorly understood. This review explores the application of computational fluid dynamics and machine learning to elucidate these mechanisms and predict clinical outcomes. Computational fluid dynamic models have been instrumental in characterizing the complex interplay between AV fistula geometry, such as anastomotic angle and curvature, and hemodynamic parameters, such as wall shear stress and oscillatory shear index. These studies consistently link disturbed flow patterns, including low wall shear stress and high oscillatory shear index, to regions prone to neointimal hyperplasia and stenosis. Concurrently, machine learning models have demonstrated significant promise in predicting AV fistula maturation, stenosis, and failure by leveraging diverse data sources, including clinical characteristics, ultrasound imaging, and acoustic bruit analysis. While powerful, the clinical utility of these computational models is often limited by small, single-center datasets, a lack of external validation, and simplifying assumptions that may not capture true physiological complexity. Future progress depends on integrating these complementary approaches, using larger and more diverse datasets, and validating models prospectively to create generalizable tools that can guide surgical planning and improve AV fistula maturation rates.

A novel method for predicting the wear rate of pipelines transporting cemented paste backfill based on wall shear stress

A personalized mechanobiology-driven multiscale model of atherosclerosis.

A comparative analysis of CFD and LBM for investigating the effects of endothelial glycocalyx on the bifurcating blood flow.

Adaptive acoustic streaming microbial system for oxytetracycline removal.

Pulmonary vascular disease (PVD) is a major contributor to morbidity in preterm infants as it is associated with a significant risk to develop pulmonary hypertension, especially in infants diagnosed with prematurity-associated lung disease (PLD), also known as bronchopulmonary dysplasia (BPD). However, the earliest events of vascular injury triggered by postnatal mechanical and oxygen-related stress remain poorly understood, largely due to the limitations of existing in vitro models. We therefore developed a biomimetic, miniaturized pulmonary in vitro perfusion (PIPE) system that integrates pathophysiologically relevant shear stress with controlled oxygen exposure for the exposure of a human coculture of pulmonary microvascular endothelial cells and pulmonary artery smooth muscle cells. Advancing the system to a triple coculture, circulating THP-1 monocytes capture early endothelial-smooth muscle-immune cell interactions. Shear stress alone induced early proliferative and extracellular matrix-related responses in endothelial cells and resulted in enhanced monocyte recruitment without disrupting barrier integrity. When combined with oxygen exposure, the model revealed a dose-dependent injury pattern: moderate hyperoxia [fraction of inspired oxygen ([Formula: see text] = 0.40)] had minimal acute effects, whereas severe hyperoxia ([Formula: see text] = 0.85) impaired endothelial barrier function, increased reactive oxygen species (ROS) production, promoted monocyte transmigration, activated apoptosis (caspase 3), and elevated soluble collagen synthesis. This dynamic in vitro system reveals early drivers in vascular injury and recapitulates key characteristics of PVD, thereby introducing a translational platform for the dissection of disease mechanisms and evaluation of therapeutic strategies targeting vascular injury in the developing lung.NEW & NOTEWORTHY We present a biomimetic, miniaturized in vitro model that replicates key features of neonatal pulmonary vascular injury. By integrating physiologically relevant cues, this platform enables early detection of injury-associated molecular markers and mechanistic interrogation of disease onset. This scalable model offers a powerful tool for studying neonatal lung vascular pathology and for accelerating the discovery of early diagnostic and therapeutic strategies.

Cells residing in, and on, the calcified periodontal bone matrix experience numerous mechanical stimuli daily. The nature of the mechanical stimuli depends on whether the mechanical triggers are physiological, e.g., arising from masticatory forces, distributed via a healthy periodontal ligament to the alveolar bone, or represent "error-loads", e.g., arising during orthodontic tooth movement or around dental implants. Mechanosensitive osteocytes mediate osteoclast and osteoblast recruitment and activity in the presence of unloading, but "error loads" can directly activate signaling pathways in osteoblasts, thereby directing osteoblast activity and accumulating the bone mass essential for a functional masticatory system. Mitogen-activated protein kinases (MAPKs) play a pivotal role in regulating osteoblast growth, differentiation, and survival. This scoping review investigates which MAPKs are rapidly (within minutes) activated in osteoblasts in response to different types of mechanical stimuli. In the discussion, we tie the activation of MAPKs to altered osteoblast number and activity and the production of signaling factors. Using the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we identified studies linking MAPKs, osteoblasts, and mechanical stress. The review included 33 in vitro studies. The findings revealed that extracellular signal-regulated kinases ERK1/2, p38, and JNK were rapidly activated in osteoblasts in response to various mechanical stimuli. Fluid flow forces, representing shear stress such as those present during mastication or orthodontic movement, activated all three MAPK branches. Substrate stretch, applied to simulate strain from mastication, induced a broad spectrum of responses. Hydrostatic pressure, often applied to reflect compression from implant loading or mastication, triggered all known MAPK pathways within an hour. In contrast, more selective stimuli such as low-intensity pulsed ultrasound and hypotonic pressure preferentially activated ERK1/2. Regardless of the stimulus, ERK1/2 was usually, and rapidly activated within minutes. In conclusion, diverse mechanical stimuli, including shear stress, substrate strain, and hydrostatic pressure, frequently, and rapidly, upregulate ERK1/2 signaling in osteoblasts. Given ERK1/2's established role in promoting osteoblast proliferation and differentiation, this early activation may help explain the localized bone formation observed under mechanical loading during orthodontic treatment, dental implant integration, or alveolar bone remodeling.

Extrusion‐based bioprinting has become increasingly common due to its high cell viability, compatibility with diverse crosslinking mechanisms, and ability to print at high cell densities with minimal cellular damage. However, most fabrication workflows still rely on trial-and-error optimization, leading to time-consuming, increased material costs, and reduced reproducibility. Here, we introduce a simple and yet robust mathematical model that predicts the extrusion pressure required for printing directly from rheological data, enabling the construction of a pressure-based printability window that reduces optimization time and resource use. The predicted pressures were further used to estimate wall shear stress, providing a pre-print assessment of safe-to-print conditions. The model achieved a 5–15% relative error compared with experimentally adjusted printing pressures across multiple nozzle types. All bioprinted constructs maintained >80% cell viability, and the predicted shear stress remained below reported thresholds for fibroblast safety, confirming the model’s reliability for guiding extrusion bioprinting.

In vitro effects of voxelotor on red blood cell senescence and rheological behavior in sickle cell anemia.

Fenestrated EndoVascular Aneurysm Repair (fEVAR) has been demonstrated to be an excellent treatment for complex abdominal aortic aneurysms. In addition to the aortic endograft, bridging stent-grafts (SG) are deployed within the renal arteries, resulting in rare but serious renal complications. This study aims to assess renal artery hemodynamic changes post-fEVAR, including the effect of respiration-induced renal deformation. Pre-fEVAR models were segmented from CT scans (patients involved in clinical trial NCT04724863), while post-fEVAR models were created from structural simulations that included respiratory-induced deformation. Computational Fluid Dynamics (CFD) simulations applied inflow velocity waveforms at the supraceliac aorta and Windkessel boundary conditions at the outlets. A dynamic mesh was implemented to reproduce renal deformation during breathing, and inspiration and expiration static configurations were analyzed. Post-fEVAR reduction in renal artery flow was detected, together with recirculation regions near the SG protrusions into the aorta. Higher time-averaged wall shear stress was observed in the unstented section of the renal arteries. The comparison between static and dynamic mesh simulations reveals that renal artery motion has negligible effect on the flow. Finally, velocity fields were compared to metrics used clinically to assess renal stenosis, to build a model for the prediction of renal complications in silico. This study evaluates the impact of renal stenting on flow, accounting for respiratory-induced deformation. It shows a minimal influence on overall hemodynamics, but significant reduction of renal flow post-fEVAR. Future studies should evaluate a patient cohort who experienced renal complications to correlate CFD metrics with post-operative clinical outcomes.

High-Frequency wall vibration correlates with growth of a vertebrobasilar dolichoectatic Aneurysm: A case study.