Search Results (1,525)

Kaolin is an abundant, low-cost filler for elastomeric compounds. The kaolin used here is primarily kaolinite, chemically clean, and contains a fine particle population. Although agglomeration is evident, it can be mitigated by appropriate physical processing and, when desired, by chemical coupling. This study evaluates kaolin in natural rubber (NR) and examines how adding bis(triethoxysilylpropyl) tetrasulfide (TESPT) during mixing affects filler–matrix compatibility, viscoelastic response, cure stability, and mechanical performance. Kaolin was structurally and morphologically characterized, and the compounds were prepared in a closed mixer coupled to a torque rheometer under controlled dispersion conditions. Part 1 assessed NR with kaolin without a coupling agent, and Part 2 assessed the NR–kaolin with TESPT added during mixing (0.5 and 5 phr). Small-amplitude oscillatory shear (SAOS) was used to probe viscoelastic behavior, while oscillating disk rheometry (ODR) and tensile tests quantified cure and mechanical properties. In Part 1, kaolin increased NR stiffness in SAOS and raised the 100% and 300% moduli by about 40% and 50%, respectively, relative to the unfilled NR compound, while reducing cure reversion from 30% to 10% at 150 °C. In Part 2, TESPT produced a threshold-like response: 0.5 phr caused only minor changes, whereas 5 phr led to pronounced stiffening and cure stabilization. At 5 phr, a low-frequency plateau in G′ below 0.1 Hz with no G′–G″ crossover was observed, accompanied by higher M_H and ΔM in ODR and reversion suppressed to 1% after 30 min. These trends indicate the formation of a more connected filler-rubber network, promoted by TESPT-assisted interfacial coupling/adhesion, while also reflecting the ability of TESPT (tetrasulfide) to contribute sulfur and modify the curing chemistry. Mechanically, kaolin produced marked stiffness increases, with the 100% and 300% moduli increasing by an additional 9% and 36%, respectively, at 5 phr TESPT. At the same time, ultimate tensile strength remained lower than that of neat NR, and elongation at break decreased slightly. Overall, adding TESPT during mixing enhances interfacial coupling and network connectivity and, at higher loading, also influences cure chemistry, yielding higher modulus and strongly improved reversion resistance without increasing ultimate tensile strength relative to neat NR. Full article

Mechano-Organ-on-Chip (Mechano-OoC) platforms are emerging as powerful microphysiological systems that place mechanical cues at the center of tumor modeling, providing a scalable and human-relevant approach to recapitulate the biophysical complexity of the tumor microenvironment. Mechanical factors such as matrix stiffness, viscoelasticity, solid stress, interstitial flow, confinement, and shear critically regulate cancer progression, metastasis, immune interactions, and treatment response, yet remain poorly captured by conventional in vitro models and are often studied separately in tumor-on-chip and mechanobiology research. In this review, we summarize recent advances in mechano-OoC technologies for cancer research, highlighting strategies that integrate engineered mechanical cues with microfluidics, tunable extracellular matrices, vascular and stromal interfaces, and dynamic loading to model tumor invasion, vascular transport, immune trafficking, and drug delivery. We also discuss emerging approaches for real-time, multimodal readouts, including sensor-integrated platforms and artificial intelligence-assisted data analysis, and outline key challenges that limit translation, such as device complexity, limited throughput, insufficient standardization, and inadequate validation against in vivo and clinical data. By organizing progress across platform engineering, sensing and readout, data standardization, and AI-driven analytics, this review provides a unified framework for advancing mechanobiology-aware tumor models and guiding the development of predictive preclinical platforms for precision cancer therapy. Full article

Silicone-based implants have been widely used in breast reconstruction but have also been associated with poorly understood complications, including pathologic foreign body responses such as capsular contracture. In this study, we leveraged 3D-printing technology to generate silicone-based implants in a novel, anatomically relevant, prepectoral rat model. We used this model to evaluate the response to an extracellular matrix-based product: ovine-derived reinforced tissue matrix (RTM). Two-piece negative molds were developed through computer-aided design and 3D-printed. The molds were filled with various polydimethylsiloxane mixtures and dip-coated to fabricate implants. Implant material characterization revealed that the implants retained the original 3D-printed mold shape and qualitatively demonstrated a shell with an inner solid gel-like structure. Fabricated implants had smooth surfaces, as well as tunable features including implant stiffness (storage modulus). From initial studies in our rat model, placement of bilateral prepectoral implants allowed assessment of both muscle- and skin-facing capsules and were well-tolerated for at least 12 weeks. Comparison of the foreign body response between RTM-covered and uncovered (control) implants in this model revealed that the capsule thickness did not differ between groups at the 12-week endpoint. However, RTM reduced contractile fibroblasts (alpha-smooth muscle actin) and macrophages (Iba1) compared to the control. Our findings suggested that RTM may improve capsule quality by attenuating cells involved in fibrosis, even when total capsule thickness remains unchanged. However, these changes to cells involved in fibrosis were only observed at this early endpoint and may not predict long-term clinical outcomes. Full article

The evolving tumor microenvironment (TME) plays a critical role in breast cancer tumorigenesis, growth, and metastatic potential. This study focuses on two key components of the TME: tumor-associated neutrophils (TANs) and the desmoplastic reaction (DR). We will analyze their multifaceted functions, emphasizing the significant mutual relationships among them, which dramatically affect disease outcomes and the effectiveness of treatments. TANs can either suppress or promote tumors, demonstrating notable functional flexibility in response to signals from their immediate environment. Concurrently, the proliferation of myofibroblasts and the extensive deposition of extracellular matrix (ECM), which characterize the DR, substantially alter the tumor’s physical properties, increasing its stiffness. This increased stiffness significantly obstructs immune system cells from accessing the tumor, ultimately limiting the effectiveness of therapies and contributing to a more clinically aggressive tumor behavior. A comprehensive understanding of the interactions among TANs, the desmoplastic stroma, and other elements of the TME is critical for developing new predictive biomarkers and establishing more effective targeted therapies. Full article

Open-hole compression (OHC) tests were carried out on non-crimp fabric (NCF) laminates with varied open-hole orientation (angle to the loading direction) and inter-hole spacing. Failure modes were documented by scanning electron microscopy (SEM), and the compressive strength was quantified. Finite element simulations in Abaqus were developed to replicate the tests, establishing a progressive-damage model for open-hole laminates under compression. Intralaminar failure was described using the three-dimensional Hashin failure criterion and a modified matrix compression criterion incorporating shear coupling effects, while interlaminar delamination was modeled with cohesive elements, enabling the simulation of damage initiation, growth, delamination, and final collapse. The results show that hole orientation and spacing have a pronounced effect on open-hole compression (OHC) strength. A spacing threshold is observed, beyond which further increases in spacing provide little additional benefit. In contrast, the apparent elastic stiffness is essentially insensitive to hole spacing and orientation. The combined intralaminar and interlaminar model successfully reproduces the characteristic mechanical response—linear elasticity followed by catastrophic failure—in good agreement with the experiments. Full article

Type 2 diabetes mellitus (T2DM) is characterized not only by chronic hyperglycemia but also by profound adipose tissue dysfunction, including impaired lipid handling, low-grade inflammation, mitochondrial dysfunction, and extracellular matrix (ECM) remodeling. These adipose tissue alterations play a central role in the development of systemic insulin resistance, ectopic lipid accumulation, and cardiometabolic complications. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), particularly semaglutide, have emerged as highly effective therapies for T2DM and obesity. While their glucose-lowering and appetite-suppressive effects are well established, accumulating evidence indicates that semaglutide exerts pleiotropic metabolic actions that extend beyond glycemic control, with adipose tissue representing a key target organ. This review synthesizes current preclinical and clinical evidence on the molecular and cellular mechanisms through which semaglutide modulates adipose tissue biology in T2DM. We discuss depot-specific effects on visceral and subcutaneous adipose tissue, regulation of adipocyte lipid metabolism and lipolysis, enhancement of mitochondrial biogenesis and oxidative capacity, induction of beige adipocyte programming, modulation of adipokine and cytokine secretion, immunometabolic remodeling, and attenuation of adipose tissue fibrosis and ECM stiffness. Collectively, available data indicate that semaglutide promotes a functional shift in adipose tissue from a pro-inflammatory, lipid-storing phenotype toward a more oxidative, insulin-sensitive, and metabolically flexible state. These adipose-centered adaptations likely contribute to improvements in systemic insulin sensitivity, reduction in ectopic fat deposition, and attenuation of cardiometabolic risk observed in patients with T2DM. Despite compelling mechanistic insights, much of the current evidence derives from animal models or in vitro systems. Human adipose tissue-focused studies integrating molecular profiling, advanced imaging, and longitudinal clinical data are therefore needed to fully elucidate the extra-glycemic actions of semaglutide and to translate these findings into adipose-targeted therapeutic strategies. Full article

Cemented granular materials (CGMs) represent a transitional class of geomaterials where mechanical behavior is governed by the interplay between a discrete granular skeleton and a continuous cementitious matrix. While previous studies have focused on idealized spherical particles, this study aims to quantify the influence of the cement filling ratio (ranging from 10% to 100%) on the mechanical constitutive behavior of CGMs fabricated with large, irregular granitic aggregates (14–20 mm). Unconfined compressive tests and splitting tensile tests were conducted to evaluate the evolution of strength, stiffness, and failure modes. The results reveal a distinct mechanical transition governed by the cement filling ratio (${\rho }_m$). The elastic modulus and splitting tensile strength exhibited a linear increase with ${\rho }_m$ (R2 > 0.95), indicating a direct dependence on the volume fraction of the binding phase. In contrast, the unconfined compressive strength (UCS) and peak strain displayed a bilinear growth pattern with a critical inflection point at ${\rho }_m$ = 80%. For the specific irregular granitic aggregate skeleton investigated, this threshold marks the transition from contact-dominated stability to matrix-dominated continuum behavior. Below this threshold, strength gain is limited by the stability of discrete particle contacts; above 80%, the material behaves as a continuum, with UCS increasing rapidly to a maximum of 41.78 MPa at 100% filling. Furthermore, the dispersion of stress–strain responses significantly decreased as ${\rho }_m$ exceeded 50%, attributed to the homogenization of stress distribution within the specimen. These findings provide a quantitative basis for optimizing cement usage in ground reinforcement applications, identifying 80% as a critical design threshold. Full article

The extracellular matrix (ECM) is a dynamic, tissue-specific network that integrates biochemical and mechanical cues to regulate cell behavior and organ homeostasis. Increasing evidence indicates that dysregulated ECM remodeling is an upstream driver of chronic human diseases rather than a passive consequence of injury. This review summarizes principles of ECM organization, mechanotransduction, and pathological remodeling and highlights translational opportunities for ECM-targeted therapies, biomaterial platforms, and precision diagnostics. We conducted a narrative synthesis of foundational and recent literature covering ECM composition and turnover, stiffness-dependent signaling, and disease-associated remodeling across fibrosis/cardiovascular disease, cancer, and metabolic disorders, together with advances in ECM-based biomaterials, drug delivery, and ECMderived biomarkers and imaging. Across organs, a self-reinforcing cycle of altered matrix composition, excessive crosslinking, and stiffness-dependent mechanotransduction (including integrin–FAK and YAP/TAZ pathways) sustains fibroinflammation, myofibroblast persistence, and progressive tissue dysfunction. In tumors, aligned and crosslinked ECM promotes invasion, immune evasion, and therapy resistance while also shaping perfusion and drug penetration. Translational strategies increasingly focus on modulating ECM synthesis and crosslinking, normalizing rather than ablating matrix architecture, and targeting ECM–cell signaling axes in combination with anti-fibrotic, cytotoxic, or immunotherapeutic regimens. ECM biology provides a unifying framework linking pathogenesis, therapy, and precision diagnostics across chronic diseases. Clinical translation will benefit from standardized quantitative measures of matrix remodeling, mechanism-based biomarkers of ECM turnover, and integrative imaging–omics approaches for patient stratification and treatment monitoring. Full article

Defect modes in phononic crystals (PnCs) provide strongly localized resonances that are essential for frequency-dependent wave filtering and highly sensitive sensing. Their functionality increases greatly when their spectral characteristics can be externally tuned without altering the structural configuration. However, existing feedback control strategies rely on laminated piezoelectric defects, which have uniform electromechanical loading that causes voltage cancellation for even-symmetric defect modes. Consequently, only odd-symmetric defect bands can be manipulated effectively, which limits multi-band tunability. To overcome this constraint, we propose a segmented piezoelectric sensor–actuator design that enables symmetry-dependent feedback at the defect site. We develop a transfer-matrix analytical framework to incorporate complex-valued feedback gains directly into dispersion and transmission calculations. Analytical predictions demonstrate that real-valued feedback yields opposite stiffness modifications for odd- and even-symmetric modes. This enables the simultaneous tuning of both defect bands and induces an exceptional-point-like coalescence. In contrast, imaginary feedback preserves stiffness but modulates effective damping, generating a parity-dependent amplification-suppression response. The analytical results closely match those of fully coupled finite-element simulations, reducing computation time by more than two orders of magnitude. These findings demonstrate that segmentation-enabled feedback provides an efficient and scalable approach to tunable, multi-band, non-Hermitian wave control in piezoelectric PnCs. Full article

Glucocorticoids are widely applied intra-articularly to alleviate inflammation and pain in osteoarthritis (OA). However, repeated administration and high local concentrations can lead to crystal deposition on the cartilage surface, contributing to chondrocyte damage and extracellular matrix (ECM) degradation, potentially accelerating OA progression. Calcium-dependent mechanosensors play a critical role in mediating catabolic responses in chondrocytes, but it remains unclear whether glucocorticoids affect chondrocyte mechanosensitivity or biomechanical properties. This in vitro study examined the dose-dependent effects of triamcinolone acetonide (TA) on chondrocyte biomechanics and mechanosensitivity. Primary human chondrocytes (N = 23) were cultured for one week with TA (2 µM–2 mM) or control medium. Cytoskeletal organization was visualized by F-actin staining (N = 6), and cellular elasticity (N = 5) was quantified via atomic force microscopy (AFM). Mechanotransduction was analyzed by Ca²⁺ imaging (Fluo-4 AM) upon AFM-based indentation (500 nN). Expression of matrix-related and mechanosensitive genes (N = 9) was assessed by qPCR. TA exposure induced a concentration-dependent reorganization of the F-actin cytoskeleton, pronounced at 0.2 mM, accompanied by a significant increase in the elastic modulus (p < 0.001). TA further augmented Ca²⁺ fluorescence intensity under basal conditions and during mechanical stimulation. Blocking cationic mechanosensitive channels with GsMtx4 (N = 3) markedly reduced the TA-evoked Ca²⁺ influx (p < 0.0001). Significant reduction in MMP1 was observed on the transcriptional level (N = 9) after TA-treatment (p < 0.05). In summary, TA enhances chondrocyte stiffness through cytoskeletal condensation and amplifies Ca²⁺-dependent mechanotransduction but reduces MMP1 expression, indicating a dual biomechanical response of chondrocytes to OA under exposure of potent corticosteroid. Full article

Glass fiber-reinforced polymer (GFRP) composites are widely used in structural applications due to their high specific strength and durability; however, their mechanical performance strongly depends on fiber architecture and environmental exposure. This study evaluates the mechanical behavior and moisture-induced degradation of GFRP laminates through tensile tests, impact tests, dynamic mechanical analysis (DMA), and thermomechanical analysis (TMA) performed on a bi-directional glass–epoxy GFRP laminate ([0°/90°]). Tensile tests revealed a maximum longitudinal strength of 369 MPa in dry specimens, while water immersion for up to 21 days led to a significant reduction in tensile strength, from 207 MPa to 63 MPa, in diagonally cut specimens. Impact tests conducted at 12 J showed larger displacements in specimens cut along directions not aligned with the fibers, indicating matrix-dominated behavior. Dynamic mechanical analysis demonstrated strong dependence of stiffness on fiber orientation, with storage modulus values decreasing by approximately 45% in 45° specimens compared with the principal directions, while the glass transition temperature remained within 59–62 °C. Thermomechanical analysis confirmed an increase in the coefficient of thermal expansion after aging, from 205.6 to 291.65 µm/(m·°C) below Tg. These results provide insights into the structure–property–environment relationships governing the durability of GFRP composites and support the optimization of their design for long-term polymer-based applications. Full article

Atrial fibrillation (AF) is the most common sustained heart rhythm disorder. It is estimated that AF affects over 52 million people worldwide, with its prevalence expected to double in the next four decades. AF significantly increases the risk of stroke and heart failure, contributing to 340,000 excess deaths annually. Beyond these life-threatening complications, AF results in limitations in physical, emotional, and social well-being causing significant reductions in quality of life and resulting in 8.4 million disability-adjusted life-years per year, highlighting the wide-ranging impact of AF on public health. Moreover, AF is increasingly recognized for its association with cognitive decline and dementia. AF is a chronic and progressive disease characterized by rapid and erratic electrical activity in the atria, often in association with structural changes in the heart tissue. AF is often initiated by triggered activity, often from ectopic foci in the pulmonary veins. These triggered impulses may initiate AF via: (1) sustained rapid firing with secondary disorganization into fibrillatory waves, or (2) by triggering micro re-entrant circuits around the pulmonary venous-LA junction and within the atrial body. In each instance, AF perpetuation necessitates the presence of a vulnerable atrial substrate, which perpetuates and stabilizes re-entrant circuits through a combination of slowed and heterogeneous conduction, as well as functional conduction abnormalities (e.g., fibrosis disrupting tissue integrity, and abnormalities in the intercalated disks disrupting effective cell-to-cell coupling). The re-entry wavelength, determined by conduction velocity and refractory period, is shortened by slowed conduction, favoring AF maintenance. One major factor contributing to these changes is the disruption of the extracellular matrix (ECM), which is induced by atrial fibrosis. Fibrosis-driven disruption of the ECM, especially in the heart and blood vessels, is commonly caused by conditions such as aging, hypertension, diabetes, smoking, and chronic inflammatory or autoimmune diseases. These factors lead to excessive collagen and protein deposition by activated fibroblasts (i.e., myofibroblasts), resulting in increased tissue stiffness, maladaptive remodeling, and impaired organ function. Fibrosis typically occurs when cardiac fibroblasts are activated to myofibroblasts, resulting in the deposition of excessive collagen and other proteins. This change in ECM interferes with the normal electrical function of the heart by creating irregular, fibrotic regions. AF and atrial fibrosis have a reciprocal relationship: AF promotes fibrosis through fibroblast activation and extracellular matrix buildup, while atrial fibrosis can sustain and perpetuate AF, contributing to higher rates of AF recurrence after treatments such as catheter ablation or cardioversion. Full article

The brain’s extracellular matrix (ECM) serves as a dynamic and instructive regulator of glioma progression. The ECM provides structural support while integrating pharmacological and mechanical signals that influence glioma initiation, progression, and treatment resistance. Deviant ECM remodeling fosters tumor heterogeneity, invasion, and immune evasion by altering stiffness, composition, and cellular matrix signaling. We proposed that ECM remodeling in gliomas not only facilitates tumor growth and heterogeneity but also establishes advantageous biophysical and metabolic conditions that foster treatment resistance and recurrence. Our objective is to analyze current findings regarding the structural, biochemical, and mechanical roles of the brain ECM in glioma growth, emphasizing its contribution to tumor heterogeneity, mechanotransduction, immunological modulation, and its potential as a therapeutic target. Method: A comprehensive literature review was conducted using scientific databases including PubMed, Web of Science, and Scopus. Peer-reviewed literature published between 2000 and 2025 was selected for its relevance to ECM composition, stiffness, remodeling enzymes, extracellular vesicles, and mechanobiological processes in gliomas. Results: Recent investigations demonstrate that glioma cells actively alter the ECM by secreting collagens, laminins, and metalloproteinases, establishing a feedback loop that facilitates invasion and resistance. Discussion: Mechanical variables, such as ECM stiffness and solid stress, influence glioma growth, metabolism, and immune exclusion. Moreover, extracellular vesicles facilitate significant extracellular matrix remodeling and improve communication between tumors and stromal cells. The disruption of ependymal and subventricular extracellular matrix niches enhances invasion and cerebrospinal fluid-mediated signaling. The remodeling of the ECM influences glioma growth through interconnected biochemical, mechanical, and immunological mechanisms. Examining ECM stiffness, crosslinking enzymes, and vesicle-mediated signaling represents a potential therapeutic approach. Integrative methodologies that combine mechanobiology, imaging, and multiomics analysis could uncover ECM-related vulnerabilities to improve glioma treatment. Full article

This work examines the impact of integrating recycled rubber particles on the dynamic mechanical properties of polyester/fiberglass (P/F) composites. Rubber particles of several mesh sizes (M20 and M40) and volume fractions (10%, 20%, and 30%) were included in the P/F composite. The findings indicate that increasing rubber content reduces density and affects the tensile strength and fracture characteristics of the composites. Rubber often decreases stiffness while potentially enhancing damping, contingent on its interaction with the polyester matrix. The P/F/M40_20% composite demonstrates significant stiffness and moderate damping, indicating a distinctive reinforcing mechanism. The relationship between rubber tensile strength and fractured behavior is complex. M40 composites weaken at 30% owing to debonding, but M20 composites only slightly decrease in strength at 20% rubber. Interestingly, M20_30% has increased strength due to rubber–fracture interactions. Fiberglass reinforcement stiffens the material but reduces vibration absorption. Rubber enhances flexibility and may attenuate vibrations. A weighted scoring method determines that the P/F/M20_20% rubber composite is the most advantageous for attaining equilibrium of toughness, strength, and damping characteristics. This work elucidates how to optimize the performance of P/F composites by modifying the properties of rubber particles for targeted applications. Full article

Magnesium matrix composites formed by incorporating ceramic particles into a magnesium alloy matrix can effectively leverage the complementary properties of the matrix and reinforcement. This approach significantly enhances the mechanical properties of the material at both room and elevated temperatures, offering a viable solution to the inherent limitations of Mg alloys, such as insufficient absolute strength, stiffness, and poor heat resistance. This article reviews the latest research progress in the field of ceramic particle-reinforced magnesium matrix composites in recent years. First, the current research status of magnesium matrix composites reinforced with different types of ceramic particles is comprehensively summarized. Subsequently, it provides a summary and in-depth analysis of the principles, key technologies, and microstructural characteristics of both mainstream and emerging preparation processes, and discusses their advantages and disadvantages. Finally, the challenges in current research are analyzed, and future cutting-edge directions for developing high-performance ceramic particle-reinforced magnesium matrix composites are discussed. Full article