Search Results (733)

Adaptive Equivalent Consumption Minimization Strategies (A-ECMSs) are one of the best methodologies to optimize fuel consumption of plug-in hybrid vehicles (PHEVs) coupled with low computational requirements. In this paper, a review of A-ECMSs is proposed. Starting from an economic-environmental contextualization, hybrid vehicles are presented and classified, together with their modeling methodologies and the physical-mathematical representation of their components. Next, the control theory for hybrid vehicles is introduced and classified, deriving the A-ECMS approach. Several works accounting for different A-ECMS implementations, based on technology integration, time horizon, adaptivity mechanism, and technique, are addressed. The literature analysis shows a broad coverage of possibilities: the simple proportional-integral (PI) rule for equivalence factor adaptivity is often used, imposing a given battery state-of-charge (SoC); it is possible to optimally plan the battery SoC trajectory through offline optimization with optimal algorithms or by predicting ahead conditions with model predictive control (MPC) or neural networks (NNs); the integration with emerging technologies such as Vehicle-To-Everything (V2X) can be helpful, accounting also for car-following data and GPS information. Moreover, speed prediction is another common technique to optimally plan the battery SoC trajectory. Depending on available on-board computational power and data, it is possible to choose the best A-ECMS according to its application. Full article

Pulmonary fibrosis is a progressive interstitial lung disease that involves stimulated growth of fibroblasts, over-deposition of extracellular matrix (ECM), and permanent damage of the lung structure. Among its various forms, idiopathic pulmonary fibrosis (IPF) is the most common and life-threatening type with few treatment options and a poor prognosis. Such obstacles highlight the urgency to find new molecular targets by better understanding the cellular and signaling processes that contribute to the pathogenesis of the disease. Chemerin is an adipokine and chemoattractant protein that has recently come into the limelight as a major controller of immune cell trafficking, inflammation, and tissue remodeling. Its biological activity is mainly mediated by binding to its receptors Chemokine-like receptor 1 (CMKLR1), G protein-coupled receptor 1 (GPR1), and C-C chemokine receptor-like 2 (CCRL2), and has been linked to numerous pathological conditions, such as metabolic diseases, cancer, and inflammatory diseases. Emerging data now indicate that chemerin can also be a key factor in the initiation and progression of pulmonary fibrosis. The aim of the review is to overview the existing evidence regarding regulatory processes of chemerin expression, signaling pathways, and effects of this protein in cells in the fibrotic lung microenvironment. Moreover, we will comment on the findings of in vitro and in vivo experiments supporting the possibility of chemerin as a promising molecular target in basic research on pulmonary fibrosis. Full article

Due to the highly nonlinear, dynamic, and slowly time-varying nature of lithium-ion batteries (LIBs) during operation, achieving accurate and real-time parameters online identification in first-order RC equivalent circuit models (ECMs) remains a significant challenge, including low accuracy and poor real-time performance. This paper establishes a fractional-order chaotic system for first-order RC-ECM based on a charge-controlled memristor. The system exhibits chaotic behavior when parameters are tuned. Then, based on the principle of the state observer, an identification observer is designed for each unknown parameter of the first-order RC-ECM, achieving online identification of these unknown parameters of the first-order RC-ECM of LIB. The proposed method addresses key limitations of traditional parameter identification techniques, which often rely on large sample datasets and are sensitive to variations in ambient temperature, road conditions, load states, and battery chemistry. Experimental validation was conducted under the HPPC, DST, and UDDS conditions. Using the actual terminal voltage of a single cell as a reference, the identified first-order RC-ECM parameters enabled accurate prediction of the online terminal voltage. Comparative results demonstrate that the proposed state observer achieves significantly higher accuracy than the forgetting factor recursive least squares (FFRLS) algorithm and Kalman filter (KF) algorithm, while offering superior real-time performance, robustness, and faster convergence. Full article

Traditional mechanical processing techniques are confronted with significant challenges when machining advanced materials possessing excellent mechanical properties. Electrochemical machining (ECM), as a material removal technology based on the principle of anodic dissolution, demonstrates distinctive advantages including the absence of contact stress, independence from material hardness, and elimination of mechanical residual stress and recast layers. These characteristics render ECM particularly suitable for high-precision applications requiring superior surface quality. This review systematically summarizes the applications, recent progress, and current challenges of ECM in surface processing. According to diverse surface requirements, ECM technology is classified into two core directions based on primary objectives. The first direction focuses on surface quality enhancement, where nanoscale planarization, residual stress reduction, and uniform surface performance are achieved through precise regulation of anodic dissolution. The second direction concerns material shaping, which is subdivided into macro-scale and micro-scale processing. Macro-scale forming combines electrochemical dissolution with mechanical action to maintain high material removal rate (MRR) while achieving micron-level precision. Micro-scale forming employs nanosecond pulse power supplies and precision electrode/mask designs to overcome manufacturing limitations of micro-nano features on hard-brittle materials. Despite progress achieved, key technical bottlenecks persist, including unstable dynamic control of the inter-electrode gap, environmental concerns regarding electrolytes, and tooling degradation. Future research should prioritize the development of green processing technologies, intelligent control systems, multi-scale manufacturing strategies, and multi-energy field hybrid technologies to enhance the capability of ECM in meeting increasingly stringent surface requirements for advanced materials. Full article

During embryonic development, angiogenesis and arteriogenesis are responsible for vast growth and remodeling. These processes have distinct mechanisms, like budding, cord hollowing, cell hollowing, cell wrapping, and intussusception. This review discusses the diversity of morphogenetic mechanisms contributing to vessel assembly and angiogenic sprouting in blood vessels and how molecular pathways regulate some complex cell behaviors concerning the VEGFR pathway. Also, a particular part is dedicated to the HIF 1α gene. The key components of the VEGFR pathway are VEGF receptors VEGFR1, VEGFR2, and VEGFR3. VEGFR2 plays a central role in vascular morphogenesis. VEGF is the primary ligand involved in angiogenesis and arteriogenesis. Various types of VEGF are being studied in terms of their therapeutic use. The ultimate goal of the vascular morphogenesis study is to enable the development of organized vascular tissue that presumably might be used to replace the diseased one. Cellular chirality—the intrinsic “handedness” of cells in movement, structure, and organization—plays a crucial role in angiogenesis, the process by which new blood vessels develop from old ones. This chiral activity is essential for the directed and patterned organization of endothelial cells during vascular formation and remodeling. In angiogenesis, cellular chirality directs endothelial cells to adopt specific orientations and migratory patterns, which are crucial for the formation of functionally organized blood vessels that provide tissues with the necessary nutrients and oxygen. Cellular chirality in this environment is affected by multiple mechanisms, including VEGF/VEGFR signaling, mechanical pressures, interactions with the extracellular matrix (ECM), and cytoskeletal movements. Lately, researchers have focused on the molecular control of blood vessel morphogenesis, the study of signaling circuitry implied in vascular morphogenesis, the emerging mechanism of vascular stabilization, and helical vasculogenesis driven by cell chirality. Full article

Preeclampsia (PE) and intrauterine growth restriction (IUGR) are major pregnancy complications that are linked to placental dysfunction and environmental stimulation such as the use of electronic cigarettes (eCig). This study investigates the molecular impacts of timed eCig exposure in a C57BL/6 mouse model of PE and IUGR using bulk RNA-sequencing of placental tissues. Pregnant mice were exposed to eCig vapor via nose-only system starting at embryonic day 12.5 (eCig-6d, before spiral artery (SA) invasion) or 14.5 (eCig-4d, after SA invasion) until E18.5 (necropsy), with healthy controls exposed to room air (n = 6/group). The eCig-4d group developed PE, whereas the eCig-6d group developed both PE and IUGR. RNA-seq analysis revealed 429 differentially expressed genes (DEGs) in eCig-4d (IUGR-like) group and 64 DEGs in eCig-6d (PE + IUGR-like) group compared to controls. Pathway and gene network analyses indicated that eCig-4d exposure activated NF-κB–driven inflammation, suppressed ECM organization and collagen biosynthesis, and downregulated vasoactive genes/mitochondrial-associated genes (NOS1/2), accompanied by impaired complement initiation and reduced both macrophage and monocyte signals. Similarly, eCig-6d exposure led to downregulation of complement-associated genes and granule-related components, possibly implicating weakened neutrophil responsiveness and compromised inflammatory resolution at the maternal–fetal interface. Our findings align with prior studies on physiological dysfunctions in PE and IUGR, while also providing novel insights into the temporally specific cellular responses induced by eCig exposure. Full article

Cardiovascular aging is a multifactorial and systemic process that contributes significantly to the global burden of cardiovascular disease, particularly in older populations. This review explores the molecular and cellular mechanisms underlying cardiovascular remodeling in age-related conditions such as hypertension, atrial fibrillation, atherosclerosis, and heart failure. Central to this process are chronic low-grade inflammation (inflammaging), oxidative stress, cellular senescence, and maladaptive extracellular matrix remodeling. These hallmarks of aging interact to impair endothelial function, promote fibrosis, and compromise cardiac and vascular integrity. Key molecular pathways—including the renin–angiotensin–aldosterone system, NF-κB, NLRP3 inflammasome, IL-6, and TGF-β signaling—contribute to the transdifferentiation of vascular cells, immune dysregulation, and progressive tissue stiffening. We also highlight the role of the senescence-associated secretory phenotype and mitochondrial dysfunction in perpetuating inflammatory and fibrotic cascades. Emerging molecular therapies offer promising strategies to reverse or halt maladaptive remodeling. These include senescence-targeting agents (senolytics), Nrf2 activators, RNA-based drugs, and ECM-modulating compounds such as MMP inhibitors. Additionally, statins and anti-inflammatory biologics (e.g., IL-1β inhibitors) exhibit pleiotropic effects that extend beyond traditional risk factor control. Understanding the molecular basis of remodeling is essential for guiding future research and improving outcomes in older adults at risk of CVD. Full article

Impaired bone regeneration and wound healing represent a major clinical and socioeconomic challenge for our aging and multimorbid population. Fracture and wound healing share many common features, with transforming growth factor beta (TGF-β) being a key regulator of inflammation, angiogenesis, fibroblast activation, and matrix remodeling. The dysregulation of TGF-β signaling is a hallmark of chronic wounds, excessive scar formation, and fracture non-union. Extracellular matrix protein 1 (ECM1) plays a crucial role in the activation of latent TGF-β. As a protein of the extracellular matrix, ECM1 offers ideal conditions for the biofunctionalization of bone implants or wound patches. Its mode of action has been studied mainly in fibrosis models of the liver or heart, where TGF-β acts as a driver of the disease. The controlled knock-out or overexpression of ECM1 either promoted or improved fibrosis development. In this review, we discuss how these findings can be applied to the biofunctionalization of implants to support bone and wound healing, considering the impact of TGF-β on the different healing phases. Full article

The extracellular matrix (ECM) supports spermatogonial stem cell (SSC) function by mimicking biochemical and structural features of the native niche. However, optimal feeder systems and ECM materials remain key limitations in porcine SSC (pSSC) cultures. We developed a porcine-derived ECM (pECM) from porcine feet and evaluated its effectiveness in supporting pSSC maintenance and proliferation under feeder-dependent conditions. We examined protein molecular weight distribution and pECM extract composition. Surface characterization was performed using scanning electron microscopy and atomic force microscopy. We compared pECM with conventional coatings, including gelatin and non-coated controls, using morphological analysis, WST-1 assay, cell cycle analysis, and gene/protein expression of SSC markers. pECM promoted larger, well-defined pSSC colonies and enhanced stemness-related marker expression, including PGP9.5, Thy-1, PLZF, GFRA1, NANOG, and VASA. Additionally, pECM facilitated active pSSC proliferation while suppressing feeder overgrowth, contributing to a stable and functional co-culture environment. Conversely, gelatin supported early feeder proliferation but led to growth saturation, whereas N/C showed delayed attachment and reduced viability. These findings suggest that pECM mimics the native SSC niche and improves pSSC culture. The dual function of pECM in regulating feeder behavior and enhancing pSSC maintenance highlights its potential as a biomaterial for species lacking established feeder-free protocols. Full article

Peptides are widely used in cosmetic formulations to stimulate extracellular matrix (ECM) synthesis, while silybin (a flavonolignan from Silybum marianum) offers retinol-like benefits through antioxidant and photoprotective activity. This study evaluated a novel anti-aging cream combining seven bioactive peptides with silybin to assess synergistic effects on ECM regeneration and clinical skin rejuvenation. In vitro assays in human dermal fibroblasts and keratinocytes revealed that the formulation rapidly upregulated gene and protein expression of collagen types I, III, IV, and XVII and lysyl oxidase (LOX) within 4–16 h. Ex-vivo, ultraviolet (UV)-damaged skin explants treated with the peptide–silybin complex showed enhanced recovery of collagen, elastic fibers, and LOX versus untreated controls. A 56-day clinical study (n = 31) demonstrated significant improvements in wrinkle area and volume, elasticity (+12.5%), firmness (+20.7%), and dermal density (+78%, all p < 0.001). No adverse effects were reported, and over 80% of participants noted improved skin texture and firmness. These findings highlight a novel synergy between peptides and silybin, with rapid ECM activation and clinical efficacy. To our knowledge, this is the first evidence of a cosmetic peptide formulation significantly upregulating LOX expression, suggesting a new mechanism for strengthening dermal architecture and improving skin resilience. Future studies should elucidate the mechanisms underlying these effects and assess whether other botanicals confer complementary benefits when combined with peptide blends. Full article

Energy management in hybrid fuel cell ship systems faces the dual challenges of optimizing hydrogen consumption and ensuring power quality. This study proposes an Improved Weighted Antlion Optimization (IW-ALO) algorithm for multi-objective problems. The method incorporates a dynamic weight adjustment mechanism and an elite-guided strategy, which significantly enhance global search capability and convergence performance. By integrating IW-ALO with the Equivalent Consumption Minimization Strategy (ECMS), an improved weighted ECMS (IW-ECMS) is developed, enabling real-time optimization of the equivalence factor and ensuring efficient energy sharing between the fuel cell and the lithium-ion battery. To validate the proposed strategy, a system simulation model is established in Matlab/Simulink 2017b. Compared with the rule-based state machine control and optimization-based ECMS methods over a representative 300 s ferry operating cycle, the IW-ECMS achieves a hydrogen consumption reduction of 43.4% and 42.6%, respectively, corresponding to a minimum total usage of 166.6 g under the specified load profile, while maintaining real-time system responsiveness. These reductions reflect the scenario tested, characterized by frequent load variations. Nonetheless, the results highlight the potential of IW-ECMS to enhance the economic performance of ship power systems and offer a novel approach for multi-objective cooperative optimization in complex energy systems. Full article

Pulmonary fibrosis (PF) is a progressive and fatal lung disease characterized by irreversible alveolar destruction and pathological extracellular matrix (ECM) deposition. Currently approved agents (pirfenidone and nintedanib) slow functional decline but do not reverse established fibrosis or restore functional alveoli. Multifunctional bioscaffolds present a promising therapeutic strategy through targeted modulation of critical cellular processes, including proliferation, migration, and differentiation. This review synthesizes recent advances in scaffold-based interventions for PF, with a focus on their dual mechano-epigenetic regulatory functions. We delineate how scaffold properties (elastic modulus, stiffness gradients, dynamic mechanical cues) direct cell fate decisions via mechanotransduction pathways, exemplified by focal adhesion–cytoskeleton coupling. Critically, we highlight how pathological mechanical inputs establish and perpetuate self-reinforcing epigenetic barriers to regeneration through aberrant chromatin states. Furthermore, we examine scaffolds as platforms for precision epigenetic drug delivery, particularly controlled release of inhibitors targeting DNA methyltransferases (DNMTi) and histone deacetylases (HDACi) to disrupt this mechano-reinforced barrier. Evidence from PF murine models and ex vivo lung slice cultures demonstrate scaffold-mediated remodeling of the fibrotic niche, with key studies reporting substantial reductions in collagen deposition and significant increases in alveolar epithelial cell markers following intervention. These quantitative outcomes highlight enhanced alveolar epithelial plasticity and upregulating antifibrotic gene networks. Emerging integration of stimuli-responsive biomaterials, CRISPR/dCas9-based epigenetic editors, and AI-driven design to enhance scaffold functionality is discussed. Collectively, multifunctional bioscaffolds hold significant potential for clinical translation by uniquely co-targeting mechanotransduction and epigenetic reprogramming. Future work will need to resolve persistent challenges, including the erasure of pathological mechanical memory and precise spatiotemporal control of epigenetic modifiers in vivo, to unlock their full therapeutic potential. Full article

β-Hydroxy-β-methylbutyrate (HMB), a natural metabolite derived from the essential amino acid leucine, is primarily recognised for its anabolic and anti-catabolic effects on skeletal muscle tissue. Recent studies indicate that HMB may also play a role in influencing the structural organisation of extracellular matrix (ECM) components, particularly collagen, which is crucial for maintaining the mechanical integrity of connective tissues. In this investigation, bovine type I collagen was polymerised in the presence of two concentrations of HMB (0.025 M and 0.25 M) to explore its potential function as a molecular modulator of fibrillogenesis. The morphology of the resulting collagen fibres and their molecular architecture were examined using atomic force microscopy (AFM) and Fourier-transform infrared (FTIR) spectroscopy. The findings demonstrated that lower levels of HMB facilitated the formation of more regular and well-organised fibrillar structures, exhibiting increased D-band periodicity and enhanced stabilisation of the native collagen triple helix, as indicated by Amide I and III band profiles. Conversely, higher concentrations of HMB led to significant disruption of fibril morphology and alterations in secondary structure, suggesting that HMB interferes with the self-assembly of collagen monomers. These structural changes are consistent with a non-covalent influence on interchain interactions and fibril organisation, to which hydrogen bonding and short-range electrostatics may contribute. Collectively, the results highlight the potential of HMB as a small-molecule regulator for soft-tissue matrix engineering, extending its consideration beyond metabolic supplementation towards controllable, materials-oriented modulation of ECM structure. Full article

Background: Type 2 diabetes (T2D) is associated with reduced cardiorespiratory fitness (CRF), a critical predictor of cardiovascular disease and all-cause mortality. CRF relies upon the coordinated action of multiple systems including the skeletal muscle where the mitochondria metabolize oxygen and substrates to sustain ATP production. Yet, previous studies have shown that impairments in muscle bioenergetics in T2D are not solely due to mitochondrial deficits. This finding indicates that factors outside the mitochondria, particularly within the local tissue microenvironment, may contribute to reduced CRF. One such factor is the extracellular matrix (ECM), which plays structural and regulatory roles in metabolic processes. Despite its potential regulatory role, the contribution of ECM remodeling to metabolic impairment in T2D remains poorly understood. We hypothesize that pathological remodeling of the skeletal muscle ECM in overweight individuals with and without T2D impairs bioenergetics and insulin sensitivity, and that exercise may help to ameliorate these effects. Methods: Participants with T2D (n = 21) and overweight controls (n = 24) completed a 10-day single-leg exercise training (SLET) intervention. Muscle samples obtained before and after the intervention were analyzed for ECM components, including collagen, elastin, hyaluronic acid, dystrophin, and proteoglycans, using second harmonic generation imaging and immunohistochemistry. Results: Positive correlations were observed with elastin content and both glucose infusion rate (p = 0.0010) and CRF (0.0363). The collagen area was elevated in participants with T2D at baseline (p = 0.0443) and showed a trend toward reduction following a 10-day SLET (p = 0.0867). Collagen mass remained unchanged, suggesting differences in density. Dystrophin levels were increased with SLET (p = 0.0256). Conclusions: These findings identify that structural proteins contribute to aerobic capacity and identify elastin as an ECM component linked to insulin sensitivity and CRF. Full article

Ozone (O₃) has re-emerged in periodontology for its antimicrobial, oxygenating, and immunomodulatory actions, yet its role in regeneration remains contentious. This narrative review synthesizes current evidence on adjunctive ozone use in periodontal therapy, delineates cellular constraints—especially in periodontal ligament fibroblasts (PDLFs)—and explores mitigation strategies using bioactive compounds and advanced delivery platforms. Two recent meta-analyses indicate that adjunctive ozone with scaling and root planing yields statistically significant reductions in probing depth and gingival inflammation, with no significant effects on bleeding on probing, plaque control, or clinical attachment level; interpretation is limited by heterogeneity of formulations, concentrations, and delivery methods. Mechanistically, ozone imposes a dose-dependent oxidative burden that depletes glutathione and inhibits glutathione peroxidase and superoxide dismutase, precipitating lipid peroxidation, mitochondrial dysfunction, ATP depletion, and PDLF apoptosis. Concurrent activation of NF-κB and upregulation of IL-6/TNF-α, together with matrix metalloproteinase-mediated extracellular matrix degradation and tissue dehydration (notably with gaseous applications), further impairs fibroblast migration, adhesion, and ECM remodeling, constraining regenerative potential. Emerging countermeasures include co-administration of polyphenols (epigallocatechin-3-gallate, resveratrol, curcumin, quercetin), coenzyme Q10, vitamin C, and hyaluronic acid to restore redox balance, stabilize mitochondria, down-modulate inflammatory cascades, and preserve ECM integrity. Nanocarrier-based platforms (nanoemulsions, polymeric nanoparticles, liposomes, hydrogels, bioadhesive films) offer controlled ozone release and co-delivery of protectants, potentially widening the therapeutic window while minimizing cytotoxicity. Overall, current evidence supports ozone as an experimental adjunct rather than a routine regenerative modality. Priority research needs include protocol standardization, dose–response definition, long-term safety, and rigorously powered randomized trials evaluating bioactive-ozone combinations and nanocarrier systems in clinically relevant periodontal endpoints. Full article