Search Results (1,326)

Traumatic brain injury (TBI) is being increasingly recognized as a major risk factor for chronic neurodegenerative disease, including chronic traumatic encephalopathy (CTE) and Alzheimer’s disease (AD). Biomechanical forces during head trauma, particularly rotational acceleration and angular deformation, produce diffuse axonal injury (DAI) and widespread white matter damage that trigger persistent neurobiological cascades. These include axonal transport failure, blood–brain barrier (BBB) disruption, neuroinflammation, neurovascular and mitochondrial dysfunction, and pathological protein aggregation, closely paralleling core AD features. Epidemiological data support a dose–response relationship between TBI severity or repetition and subsequent dementia risk, moderated by genetic factors such as apolipoprotein E4 (ApoE4). Converging experimental and early clinical studies have begun to target shared injury and neurodegenerative pathways through acute neuroprotection, stem cell-based strategies for BBB restoration and neural repair, transcriptional and hormonal modulation, mitochondrial stabilization, and immunomodulation of chronic inflammation. This review synthesizes evidence linking biomechanical injury to molecular and neurovascular pathways of neurodegeneration and summarizes emerging temporally targeted interventions. By integrating mechanistic and therapeutic perspectives, we aim to narrow the translational gap between TBI and AD, refine identification of at-risk populations, and inform priorities for prevention and development of disease-modifying therapies. Full article

The management of operating rooms (ORs) is one of the most studied topics in operations research applied to healthcare. In particular, scheduling elective surgeries in a pediatric and teaching hospital can be a challenge because disruptions occur frequently. The aim of our research was to create a mathematical programming model to schedule day hospital (DH) patients, considering possible disruptions and defining how to best manage the rescheduling process. Our study originates from a collaboration between a high-volume pediatric surgery department and operations research practitioners. The possible disruptions we consider are emergencies and same-day cancellations of planned hospital operations. Elective DH surgeries are scheduled considering the waiting list and the patients’ clinical priorities, generating a nominal schedule. This schedule is optimized in conjunction with a series of back-up schedules to guarantee that OR activity immediately recovers in case of a disruption. An ILP-based approach to the problem is proposed. We enumerate a representative subset of the possible emergency and no-show scenarios, and for each of them a back-up plan is designed. The approach reschedules patients, minimizing disruptions with respect to the nominal schedule, and applies an as-soon-as-possible policy in case of emergencies to ensure that all patients receive timely care. The approach is shown to be effective in managing disruptions, ensuring that the waiting list is managed properly, with a balanced mix of urgent and less urgent patients. It provides an effective solution for scheduling patients in a pediatric hospital, considering the unique features of such facilities. Full article

Aging profoundly reshapes the immune system, leading to increased susceptibility to infection, impaired vaccine responses, chronic inflammation, and age-associated inflammatory diseases. While immune aging has traditionally been attributed to defects in immune cell development, signaling, and metabolism, emerging evidence highlights dysregulation of programmed cell death as a central and unifying mechanism. Apoptosis, necroptosis, pyroptosis, and ferroptosis are increasingly recognized not only as terminal cellular events but also as active regulators of immune homeostasis and inflammatory signaling. In aged immune cells, coordination among these death pathways is disrupted, weakening apoptotic resolution and favoring inflammatory forms of cell death that amplify tissue damage and sustain inflammaging. In this review, we summarize current evidence on how aging remodels programmed cell death pathways in the immune system, discuss the molecular mechanisms underlying this network-level shift, and consider potential strategies for restoring immune function by modulating cell death decisions. Full article

CPVG (Utility-scale photovoltaic generation) is expanding rapidly worldwide, yet its cumulative ecological effects remain insufficiently quantified. This review synthesizes current evidence to clarify how CPVG influences ecosystems through linked mechanisms of energy redistribution, biogeochemical cycling disturbance, and ecological responses. CPVG alters surface radiation balance, modifies microclimate, and disrupts carbon–nitrogen–water fluxes, thereby driving vegetation shifts, soil degradation, and biodiversity decline. These impacts accumulate across temporal scales—from short-term construction disturbances to long-term operational feedbacks—and propagate spatially from local to regional and watershed levels. Ecological outcomes differ substantially among deserts, grasslands, and agroecosystems due to contrasting resilience and limiting factors. Based on these mechanisms, we propose a multi-scale cumulative impact assessment framework integrating indicator development, multi-source monitoring, coupled modelling, and ecological risk tiering. A full-chain mitigation pathway is further outlined, emphasizing optimized siting, disturbance reduction, adaptive management, and targeted restoration. This study provides a systematic foundation for evaluating and regulating CPVG’s cumulative ecological impacts, supporting more sustainable solar deployment. Full article

Heat damage is a common phenomenon that often occurs when drying and straightening hair. After heat damage, the hydrophobic barrier on the hair’s surface becomes disrupted, thereby altering the hair’s hydrophilicity. Meanwhile, during the process of heat damage, the rupture of the hair’s cuticles causes the hair to become dry and rough, with a decrease in gloss and a decline in mechanical properties. This study utilized epoxy silane and hydrolyzed wool keratin to synthesize a thermally responsive organic silicon-modified keratin (OSK) to prevent hair from heat damage. OSK was synthesized from epoxy silane and hydrolyzed keratin, with yield determined by quantifying free amino groups. Its hair-care performance was evaluated through assessments of hair surface morphology, mechanical properties, and optical gloss, and by combing test and contact angle measurements. Mechanisms underlying surface hydrophobicity and hair scale protection were investigated using FTIR, XPS, and DSC. Specific performance parameters were evaluated using a single-fiber strength tester and a multifunctional hair-testing instrument. FTIR confirmed successful covalent grafting, with synthesis optimized to a 90.67% yield. OSK forms a protective film on hair surfaces, verified by SEM, XPS, and TEM, restoring damaged hair hydrophobicity to a 117° contact angle and enhancing thermal protection to 136° upon heating. Beyond hydrophobic-barrier restoration, OSK improved hair gloss by 30.26% and reduced frizz by 39.33%, while restoring the key performance of virgin hair. It also provides exceptional water-repellency protection and sensory enhancement. Under thermal stress, the protective film mechanically increased tensile strength by 6.58% and yield zone tensile force by 4.65%. This article demonstrates that OSK is an effective heat-sensitive agent. When damaged by heat sources such as hair dryers, it will form a protective film on the surface of the hair, thereby protecting the surface properties of the hair. Full article

Power distribution systems face increasing threats from high-impact, low-probability (HILP) events caused by extreme weather conditions such as floods, typhoons, droughts, and heatwaves. These events often lead to power outages worldwide, highlighting the need for effective strategies to mitigate their impact. This work proposes an emergency response strategy that integrates network reconfiguration (NR) with the deployment of mobile emergency generators (MEGs) to enhance system resilience. The objective is to maximize power supply availability following HILP events. To achieve this, mixed-integer quadratic constraint programming (MIQCP) is used to optimize MEG deployment and network restoration. Additionally, improved quantitative resilience metrics are introduced to assess system degradation, pre-recovery, and recovery phases, enabling continuous resilience measurement and informed decision-making. Furthermore, an optimal capacity deployment strategy (OCDS) is proposed to ensure that MEGs are deployed with suitable capacities based on the specific needs of outage-affected areas. The effectiveness of the proposed strategy is demonstrated through tests on the IEEE 118 bus system. The results show a significant improvement of up to 100% in system resilience, reducing power outages and accelerating restoration. The findings confirm that integrating NR with optimized MEG deployment enhances service restoration, providing an effective approach for utilities to manage power disruptions. Full article

Cisplatin is an effective chemotherapeutic agent, yet its clinical utility is limited by dose-dependent nephrotoxicity. Alpha-1 antitrypsin (AAT) has cytoprotective, anti-inflammatory, and antiapoptotic properties, but its therapeutic potential in cisplatin-induced acute kidney injury (AKI) remains unclear. A murine cisplatin–AKI model was used to evaluate whether AAT (80 mg/kg) ameliorates renal injury. Renal function, oxidative stress, NADPH oxidase (NOX) isoforms, mitochondrial metabolism, inflammatory mediators, apoptosis, and fibrosis-related markers were assessed using biochemical, histological, immunohistochemical, and Western blot analyses. Cisplatin markedly impaired renal function and induced tubular injury; meanwhile, AAT significantly reversed these changes. Cisplatin also induced severe oxidative stress and disrupted the balance of NOX isoforms; AAT restored redox homeostasis. Cisplatin upregulated CPT1A/PDK4 and suppressed CPT2, UCP3, PGC1α, and DRP1, inducing maladaptive mitochondrial changes, indicating impaired β-oxidation and defective mitochondrial dynamics; AAT reversed these alterations, restoring normal mitochondrial metabolism. IL-1β, IL-6R, OPN, and F4/80 expression, recovery of the Bax/Bcl-2 ratio, and MAPK activation were reduced, indicating decreased inflammation and apoptosis; profibrotic markers were also reduced. AAT confers multifaceted protection against cisplatin-induced AKI by restoring redox balance, mitochondrial homeostasis, and inflammatory and apoptotic signaling. These findings support AAT as a promising therapeutic agent for preventing cisplatin nephrotoxicity. Full article

Background: This study examined how patients and caregivers perceive and experience AI-based care technologies through text mining analysis. The goal was to identify major themes, sentiments, and value-oriented interpretations embedded in their narratives and to understand how these perceptions align with key dimensions of patient-centered care. Methods: A corpus of publicly available narratives describing experiences with AI-based care was compiled from online communities. Natural language processing techniques were applied, including descriptive term analysis, topic modeling using Latent Dirichlet Allocation, and sentiment profiling based on a Korean lexicon. Emergent topics and emotional patterns were mapped onto domains of patient-centered care such as information quality, emotional support, autonomy, and continuity. Results: The analysis revealed a three-phase evolution of care values over time. In the early phase of AI-mediated care, patient narratives emphasized disruption of relational care, with negative themes such as reduced human connection, privacy concerns, safety uncertainties, and usability challenges, accompanied by emotions of fear and frustration. During the transitional phase, positive themes including convenience, improved access, and reassurance from diagnostic accuracy emerged alongside persistent emotional ambivalence, reflecting uncertainty regarding responsibility and control. In the final phase, care values were restored and strengthened, with sentiment patterns shifting toward trust and relief as AI functions became supportive of clinical care, while concerns related to depersonalization and surveillance diminished. Conclusions: Patients and caregivers experience AI-based care as both beneficial and unsettling. Perceptions improve when AI enhances efficiency and information flow without compromising relational aspects of care. Ensuring transparency, explainability, opportunities for human contact, and strong data protections is essential for aligning AI with principles of patient-centered care. Based on a small-scale qualitative dataset of patient narratives, this study offers an exploratory, value-oriented interpretation of how relational care evolves in AI-mediated healthcare contexts. In this study, care-ethics values are used as an analytical lens to operationalize key principles of patient-centered care within AI-mediated healthcare contexts. Full article

In marine hot–humid and salt spray environments, shipborne snap-action limit switches operating under micro-current loads are prone to triggering failures caused by the accumulation of heterogeneous films on electrical contact interfaces, which can induce abnormal behavior in electromechanical systems. To address this issue, this study systematically investigates the failure mechanisms of micro-current limit switches using multimodal diagnostic approaches. The results demonstrate that the migration and accumulation of corrosion products and foreign contaminants within the microswitch unit promote the formation of high-resistance heterogeneous films at the electrical contact interfaces, severely impairing reliable electrical conduction. Electrical contact experiments further reveal that the contact behavior is strongly dependent on the current magnitude. When the current exceeds 2A, arc discharge generated during contact closure can effectively disrupt and remove the heterogeneous films, thereby restoring the electrical functionality of previously failed switches under subsequent micro-current operating conditions. Based on the identified failure mechanism, and inspired by the natural eye-cleaning behavior of crabs, a biomimetic press-and-wipe self-cleaning dual-redundant limit switch design is proposed. The design enables autonomous surface cleaning through controlled reciprocal wiping between the moving and stationary electrical contacts, effectively suppressing the formation and accumulation of high-resistance films at the source. Comparative salt spray and damp heat storage tests demonstrate that the proposed self-cleaning limit switch maintains stable and reliable electrical contact performance in simulated marine environments, significantly improving operational reliability and service life under micro-current loads. This work provides both mechanistic insights and a practical structural solution for enhancing the reliability of electrical contact components operating under low-current conditions in harsh marine environments. Full article

Escherichia coli O157:H7 is a pathogenic bacterium that causes severe intestinal infections characterized by inflammation and disruption of the intestinal barrier. Probiotic lactic acid bacteria (LAB) from milk can support intestinal health and combat enteric pathogens; however, the potential of feline milk-derived LAB against E. coli O157:H7 infection remains unclear. In this study, Pediococcus acidilactici (P. acidilactici) M22, isolated from feline milk, was evaluated for probiotic activity in vitro and in vivo in a C57BL/6 mouse model of Escherichia coli O157:H7 infection. In vitro assays demonstrated that M22 significantly inhibited the adhesion of Escherichia coli O157:H7 to intestinal epithelial cells. For in vivo assessment, C57BL/6 mice were orally administered M22 prior to infection with E. coli O157:H7. Protective effects were evaluated by monitoring body weight loss, colon length, disease activity index (DAI), myeloperoxidase (MPO) activity, cytokine levels, tight junction protein expression, oxidative stress markers, and gut microbiota composition. M22-treated mice exhibited significantly less body weight loss and lower DAI scores than infected controls. M22 also prevented colon shortening, indicating reduced colonic damage. Probiotic treatment attenuated neutrophil infiltration and mucosal inflammation, as evidenced by decreased colonic MPO activity, reduced levels of pro-inflammatory cytokines, and elevated anti-inflammatory IL-10. Additionally, M22 preserved intestinal barrier function by upregulating tight junction proteins and mitigating infection-induced histopathological changes. M22 supplementation enhanced antioxidant defenses in colonic tissue (lower malondialdehyde, higher superoxide dismutase and glutathione), indicating reduced oxidative stress. Furthermore, gut microbiota analysis (16S rRNA sequencing) revealed that M22 counteracted infection-induced dysbiosis, restoring microbial diversity and a healthy composition (enrichment of beneficial commensals and suppression of harmful bacteria). By safeguarding intestinal integrity and homeostasis, M22 emerges as a promising next-generation probiotic for improving intestinal health in companion animals. Full article

Alterations in mitochondrial fusion and fission dynamics are critical determinants of cellular fate. However, how stress-induced mitochondrial fusion and fission affect the physiological and pathological processes in cardiomyocytes remains poorly understood. Based on an established in vitro model of stress-induced cardiomyocyte injury using isoproterenol-treated H9c2 cells, this study aimed to investigate whether the dysregulation of mitochondrial dynamics—specifically, an imbalance between fusion and fission—activates the IRE1α-ASK1-JNK endoplasmic reticulum stress signaling pathway, thereby contributing to cardiomyocyte damage. Under this experimental paradigm, cell viability was evaluated using the CCK-8 assay. Concurrently, immunofluorescence staining was employed to assess reactive oxygen species accumulation, the expression of key mitochondrial fusion/fission proteins, and components of the ER stress pathway (IRE1α, ASK1, and JNK). Results demonstrated that isoproterenol treatment elevated intracellular ROS levels and induced significant changes in both mitochondrial dynamics-related proteins and the IRE1α-ASK1-JNK signaling axis. In contrast, administration of the mitochondrial fission inhibitor Mdivi-1 attenuated ROS accumulation, restored the expression of the affected proteins toward normal levels, and alleviated cardiomyocyte injury. Collectively, these findings indicate that the disruption of mitochondrial fusion/fission dynamics triggers endoplasmic reticulum stress via the IRE1α-ASK1-JNK cascade, which participates in the pathological progression of cardiomyocyte injury. Full article

Wind turbines operate in harsh environments where leading-edge blade erosion from particulates like sand, rain, and insects is prevalent, significantly degrading aerodynamic performance and reducing power output. To counteract this, this study proposes a novel flow-control method using detached micro-cylinders placed upstream of the leading edge of eroded S809 (a wind turbine blade profile) airfoils. The approach is inspired by the concept of symmetry recovery in disturbed flows, where strategically introduced perturbations can restore balance to an asymmetric separation pattern. The aerodynamic performance of the S809 airfoil was numerically investigated under three leading-edge erosion depths (0.2%, 0.5%, and 1% of chord length, *c*) with a fixed micro-cylinder diameter of 1% *c* positioned at fifteen different locations. Findings reveal that the strategic placement of micro-cylinders ahead of the leading edge or on the pressure side markedly enhances the aerodynamic efficiency of airfoils with 0.2% and 0.5% erosion, achieving a maximum improvement of 148.7% in the lift-to-drag ratio (L/D) difference function for the 0.5% eroded airfoil. This performance recovery is interpreted as a partial restoration of flow symmetry, disrupted by erosion-induced separation. The interaction between the cylinder wake and the spill-over stall vortex originating from the erosion groove was identified as the primary mechanism, injecting high-energy fluid into the boundary layer to suppress flow separation. This study systematically parametrizes the effect of erosion depth and cylinder placement, offering new insights for mitigating erosion-induced performance loss through controlled asymmetry introduction. Full article

Background and Clinical Significance: Scurvy, caused by chronic vitamin C deficiency, is re-emerging in Western countries, particularly among pediatric patients with highly selective diets. While its musculoskeletal and mucocutaneous manifestations are well-known, its association with pulmonary arterial hypertension (PAH) is rare and poorly understood. Ascorbic acid and iron are essential cofactors for prolyl hydroxylases (PHD), which regulate Hypoxia-Inducible Factors. Their combined deficiency may trigger a “pseudohypoxic” state, leading to pulmonary vascular remodeling and vasoconstriction. Case Presentation: A 30-month-old female presented with a one-month history of limping, lower limb pain, and gingival hypertrophy. Dietary history revealed an almost exclusive cow’s milk-based intake. Physical examination showed diffuse petechiae, pallor, and right knee edema. Laboratory findings confirmed scurvy (undetectable vitamin C), severe iron-deficiency anemia (Hb: 72 g/L; ferritin: 22 mcg/L; RDW: 30%), folate deficiency, and hyperhomocysteinemia. Notably, elevated copper and vitamin B12 levels suggested a state of metabolic dysregulation. Echocardiography revealed moderate PAH phenotype (estimated sPAP: 47–50 mmHg) and a hyperdynamic contractility. A “perfect storm” mechanism was hypothesized, involving iron–ascorbate-dependent PHD impairment, high-output state, and oxidative-stress-induced hepcidin dysregulation (suggested by elevated copper). Following intravenous vitamin C and multivitamin supplementation, pulmonary pressures normalized within one week. Conclusions: PAH phenotype in scurvy represents a reversible metabolic disruption of pulmonary vascular tone rather than a structural disease. This case underscores the synergistic role of vitamin C, iron, and folate in vascular homeostasis. Clinicians should maintain high suspicion for scurvy in children with selective diets and unexplained PAH, as nutritional restoration is curative. Full article

Background: Intrauterine Growth Restriction (IUGR) is associated with a distinct neonatal metabolic profile, attributable to chronic intrauterine nutritional deprivation and suboptimal placental nutrient exchange. Upon delivery, IUGR neonates typically present with depleted nutrient stores, dysregulated endocrine activity, and a spectrum of micronutrient deficiencies, factors that collectively compromise metabolic homeostasis and significantly influence subsequent health trajectories. Methods: This narrative review systematically synthesizes the current body of evidence from clinical, biochemical, and translational investigations pertaining to the micronutrient status and pivotal endocrine markers in neonates affected by intrauterine growth restriction. The collected findings were integrated to elucidate metabolic adaptation mechanisms, immediate clinical ramifications, and the potential pathways linking neonatal biochemical patterns to long-term metabolic programming. Results: IUGR neonates consistently exhibit reduced cord-blood concentrations of essential micronutrients, including vitamin D, iron (Fe), zinc (Zn), magnesium (Mg), folate (vitamin B9), and cobalamin (vitamin B12), reflecting compromised placental nutrient transfer and limited fetal reserves. Concomitantly, endocrine alterations—most notably reduced insulin (INS) and C-peptide (C-pep) levels—indicate suppressed pancreatic β-cell activity and a prevailing hypoanabolic adaptive state. In parallel, disturbances in mineral metabolism, characterized by lower calcium (Ca) concentrations and increased alkaline phosphatase (ALP) activity, suggest impaired bone mineralization during the critical phase of early postnatal adaptation. Collectively, these biochemical patterns increase vulnerability to early clinical complications such as neonatal hypoglycemia and bone demineralization, disrupt early growth trajectories, and are associated with an elevated long-term risk of insulin resistance and adverse cardiometabolic programming. Conclusions: IUGR neonates consistently demonstrate a synergistic interplay of micronutrient deficiencies and adaptive endocrine responses, profoundly impacting immediate postnatal metabolic stability and predisposing them to long-term health challenges. Therefore, early biochemical screening, followed by tailored nutritional and hormonal interventions, may assist restore metabolic balance, promote growth and decrease long term risk for metabolic diseases. Full article

The human gut microbiome is a complex ecosystem integral to host health, with butyrate-producing bacteria (BPB) playing a critical role in maintaining intestinal homeostasis. This scoping review explores the composition, function, and systemic influence of BPB, focusing on their metabolic product, butyrate, and its implications for gut integrity, immune modulation, and gut–brain axis (GBA) communication. Disruptions to BPB abundance, which is correlated with Western dietary patterns, food additives, and antibiotic exposure, are linked to gut dysbiosis and associated with a wide spectrum of chronic diseases, including inflammatory bowel disease (IBD), obesity, type 2 diabetes, neurodegenerative disorders, and psychiatric conditions. Butyrate supports colonocyte energy metabolism, reinforces epithelial barrier function, regulates goblet cell mucus production, and exerts anti-inflammatory effects via histone deacetylase inhibition and G-protein-coupled receptor signaling. The depletion of BPB and the resultant butyrate deficiency may represent a unifying pathophysiological mechanism underlying these conditions. Therapeutic strategies that restore BPB populations and butyrate levels, such as prebiotics, dietary fiber, and microbiota-targeted interventions, hold promise for mitigating inflammation and enhancing systemic health through microbiome modulation. Full article