Search Results (597)

Atrial fibrillation (AF) is the most common supraventricular arrhythmia in adults, with a rising prevalence and a significant impact on quality of life and major cardiovascular outcomes. While atrial structural and electrical remodeling have long been central to AF pathophysiology, increasing evidence highlights the importance of psychological and mental health factors throughout the disease course. Depression, anxiety, and chronic stress are highly prevalent among individuals with AF and are associated with increased symptom burden, impaired quality of life (QoL), reduced treatment adherence, lower utilization of evidence-based therapies, and adverse clinical outcomes. Conversely, the diagnosis of AF itself may contribute to psychological distress, highlighting a complex bidirectional relationship between mental health and AF. This review summarizes current evidence on this interplay, with a focus on underlying mechanisms, including autonomic dysfunction and inflammation. Furthermore, the influence of mental health on outcomes and therapeutic strategies, and the clinical relevance of a multidisciplinary approach in contemporary AF management, are also examined. Full article

Pediatric disorders of gut–brain interaction (DGBIs) comprise chronic or recurrent symptom-based gastrointestinal conditions that cannot be fully explained by identifiable structural, biochemical, or organic abnormalities after appropriate clinical evaluation. The term DGBI is used throughout this review in accordance with current terminology, whereas the historical term “functional gastrointestinal disorders” (FGIDs) is retained only when referring to studies that used earlier Rome classifications. This review examines the impact of four modifiable factors—sleep, psychological stress, circadian rhythm, and diet—on their development and severity in children and adolescents. Relevant literature was identified through PubMed, with emphasis on recent pediatric studies, systematic reviews, and meta-analyses. Sleep disturbances are associated with greater abdominal pain, functional disability, and impaired daytime functioning. Stress may exacerbate symptoms through hypothalamic–pituitary–adrenal axis activation, autonomic imbalance, altered motility, and visceral hypersensitivity. Circadian disruption may affect gastrointestinal motility, barrier function, enteroendocrine signaling, and microbial rhythmicity, although pediatric evidence remains limited. Diet influences fermentation, microbiota, intestinal permeability, and symptom expression, with regular meals, adequate hydration, and appropriate fiber intake representing important initial measures. These factors interact bidirectionally through shared neuroendocrine, autonomic, immune, and microbial pathways. Clinical management should therefore adopt a biopsychosocial, multidisciplinary approach combining symptom management with modification of sleep, stress, circadian habits, and dietary patterns. Further prospective pediatric studies are needed to clarify causality and support personalized interventions. Full article

Coronary slow flow (CSF) is delayed distal contrast transit on angiography without flow-limiting stenosis; disturbed sleep may impair vascular control through autonomic, endothelial, inflammatory, and metabolic pathways. We evaluated Pittsburgh Sleep Quality Index (PSQI)-based sleep quality in relation to TIMI frame count (TFC)-defined CSF. This cross-sectional study enrolled 307 adults with nonobstructive coronary arteries undergoing angiography for chest pain; PSQI referenced the preceding month, and CSF was defined by corrected TFC > 27 frames in any major vessel; 132 participants had CSF and 175 normal flow. Global PSQI score was higher in CSF (median 7.0 vs. 5.0) and poor sleep quality (score > 5) was more frequent (75.8% vs. 49.7%; both p < 0.001). The global score correlated with mean TFC overall but not within flow groups. Each PSQI point independently raised CSF odds, including after STOP-Bang adjustment, although discrimination was modest. Sleep latency and short duration raised CSF odds; poor efficiency did not. Poorer sleep quality was independently linked to this angiographic slow-flow phenotype, mainly differentiating flow categories rather than tracking frame-count burden. Because coronary microvascular function was not measured directly, these hypothesis-generating findings should prompt systematic sleep assessment and prospective studies integrating objective sleep measures with invasive coronary physiology. Full article

Chronic pain is one of the most common and disabling complications of chronic kidney disease (CKD), yet it is almost exclusively viewed as a consequence of declining kidney function. This perspective overlooks the possibility that chronic pain itself may influence the biological processes driving CKD progression. Chronic pain is being recognized as a systemic disorder characterized by sustained neuroimmune activation, inflammation, oxidative stress, endothelial dysfunction, autonomic imbalance, mitochondrial impairment and maladaptive behavioral changes. These same mechanisms are also central to progressive kidney injury, raising the possibility that persistent pain may reinforce established pathogenic pathways rather than simply accompany them. We propose a conceptual framework in which chronic pain functions as a disease modifier capable of amplifying the biological and clinical processes that contribute to CKD progression. Although this hypothesis does not imply that chronic pain directly causes CKD or that pain management is inherently renoprotective, it provides a biologically plausible rationale for investigating whether pain contributes to disease progression beyond serving as a marker of disease severity. Exploring this possibility may broaden current concepts of CKD progression and identify new directions for mechanistic, translational and clinical research. Full article

Visible light communication (VLC) has emerged as a transformative optical wireless technology for sixth-generation (6G) networks, offering license-free spectrum access, inherent electromagnetic-interference immunity, high spatial confinement, and the unique ability to combine high-speed wireless connectivity with solid-state lighting infrastructure. However, the transition from conventional VLC links to practical 6G optical wireless systems requires far more than advanced modulation and signal processing. Future VLC performance will be strongly determined by the co-design of photonic front-ends, including high-speed transmitters, spectrally engineered emitters, reconfigurable optical interfaces, intelligent receivers, and energy-autonomous detection units. This article provides a comprehensive, device-centered review of photonic hardware and artificial intelligence (AI) enablers for next-generation 6G VLC systems. Particular attention is given to micro-LEDs, laser diodes, color-conversion materials, including perovskite quantum dots, advanced photodetectors, imaging receivers, wavelength-shifting fiber receivers, solar-cell-based receivers, optical reconfigurable intelligent surfaces (RISs), metasurfaces, beam-steering components, and optical wireless power transfer. This review discusses how AI can support inverse photonic design, transmitter and receiver calibration, nonlinear impairment mitigation, channel-aware beam control, and energy-aware resource management. Unlike broader VLC surveys that mainly emphasize network architecture, this article provides a device-centered perspective on AI-enabled photonic integration for 6G VLC, supported by a comprehensive survey of recent experimental demonstrations. Key challenges related to bandwidth, optical efficiency, receiver field of view, mobility, safety, standardization, and practical deployment are summarized, followed by a research roadmap for 2025–2032. Full article

Background: Parkinson’s disease (PD) exhibits remarkable clinical heterogeneity, with substantial variability in motor progression, cognitive decline, and the development of non-motor manifestations. Although the propagation of pathological alpha-synuclein is considered a central mechanism of PD pathogenesis, it does not fully explain why specific neuronal populations demonstrate differential susceptibility to degeneration. Emerging evidence suggests that selective neuronal vulnerability is determined by the interaction of multiple biological domains, including calcium homeostasis, mitochondrial bioenergetic capacity, lysosomal function, axonal architecture, synaptic resilience, and neuroinflammatory responses. Methods: A structured critical narrative review was performed using PubMed/MEDLINE, Scopus, and Web of Science databases from inception to March 2025. Only full-text articles published in English and peer-reviewed journals were included. Evidence from human post-mortem studies, genetic analyses, biomarker investigations, experimental models, induced pluripotent stem cell studies, and longitudinal clinical cohorts were systematically synthesised to identify the principal mechanisms underlying selective neuronal vulnerability and their potential translational application. To capture evidence published after this electronic cut-off, a supplementary manual review of reference lists of key systematic reviews and landmark publications was conducted up to the date of manuscript submission; references with 2025 or 2026 publication dates entered through this supplementary process. The supplementary manual review was conducted as a targeted scan of reference lists of key systematic reviews and high-impact publications identified during the primary search and did not constitute an independent updated systematic search. Results: Five interconnected biological domains emerged as key determinants of neuronal susceptibility in PD: calcium-mediated metabolic stress associated with autonomous pacemaker activity, mitochondrial dysfunction and energetic failure, impaired lysosomal degradation and proteostasis (particularly involving the GBA1–glucocerebrosidase pathway), vulnerability related to extensive axonal and synaptic architecture, and neuroinflammatory mechanisms involving microglial and astrocytic activation. Among these domains, the lysosomal pathway currently provides the strongest translational link between molecular mechanisms and measurable clinical outcomes. Based on this integrated framework, we propose the Parkinson’s Vulnerability Index (PVI), a hypothesis-generating multidimensional model combining genetic, enzymatic, alpha-synuclein seeding, cognitive, olfactory, and neuroimaging biomarkers to facilitate biological stratification and improve the design of mechanism-targeted clinical trials. Conclusions: Selective neuronal vulnerability provides a complementary framework to alpha-synuclein propagation models for understanding the heterogeneity of PD. The proposed PVI is not intended as a diagnostic or prognostic clinical instrument but as a research tool requiring prospective validation. Future precision medicine approaches in PD may benefit from integrating vulnerability-related biomarkers with existing biological staging systems to identify patients most likely to benefit from targeted disease-modifying therapies. Full article

Ankle injuries may lead to severe complications, including chronic instability and reduced mobility. Rehabilitation therefore plays a critical role in restoring normal ankle function and preventing long-term impairment. However, conventional manual physiotherapy presents several limitations, such as limited availability of therapists, variability in treatment, and reduced accessibility for home-based rehabilitation. Consequently, significant research efforts have been devoted to the development of robotic and mechatronic devices for ankle rehabilitation. In this work, we propose the design of a simple and cost-effective parallel mechanism dedicated to ankle rehabilitation. The proposed device is based on a closed-chain kinematic architecture capable of reproducing the three principal rotational degrees of freedom of the ankle joint. This configuration enables controlled and repeatable rehabilitation exercises while ensuring mechanical stability and compactness. Furthermore, the device is designed to allow patients to perform rehabilitation exercises autonomously, without the continuous assistance of a physiotherapist, both in clinical environments and in home-based rehabilitation settings. Full article

With the rapid development of edge intelligence and autonomous unmanned systems, multimodal learning has been increasingly applied to resource-constrained distributed scenarios. However, dynamic environments often introduce modality missingness, quality degradation, and reliability fluctuations, which impair learning robustness. Existing methods mainly rely on complex fusion architectures or reactive compensation strategies based on current modality states, making it difficult to satisfy the real-time and proactive requirements of edge systems. To address this issue, this paper proposes a Prediction-Driven Collaborative Compensation method for Dynamic Multimodal Quality Evolution (PDCC). Instead of reconstructing missing modality features, PDCC introduces a lightweight prediction mechanism based on historical modality confidence sequences to estimate future modality reliability trends. Based on the predicted degradation risks, a prediction-aware confidence collaboration strategy is designed to adaptively adjust reliability estimation, collaborative decisions among neighboring nodes, and replay buffer management by estimating future compensation utility from predicted modality reliability under limited storage resources. Extensive experiments on the CREMA-D and AVE datasets demonstrate that PDCC achieves strong robustness under gradual degradation, abrupt degradation, and heterogeneous multi-node degradation scenarios. Compared with existing state-driven collaborative compensation methods, PDCC improves model convergence efficiency while maintaining low communication overhead through lightweight confidence-level interactions. The results validate that the proposed method improves learning robustness in resource-constrained edge intelligence scenarios under dynamic multimodal quality evolution. Full article

Lidar systems are of major importance for driver assistance systems and autonomous driving, but their obstacle detection range can be heavily impaired by adverse weather conditions like fog. To mitigate the effects of fog, the use of polarized light has been proposed. We simulated a polarized lidar system, taking Mie theory-based scattering functions for different fog types at several wavelengths into account, and investigated the possible increase in contrast between fog backscattering and target returns for different surface types, depending on the target orientation and the polarizer configuration. Fog is modeled as an infinite, homogeneous, scattering, and absorbing medium. The simulated detector registers the time-dependent radiance, resolved by scattering order. Our findings show that the suitable choice of illumination and detection polarization allows the amount of single-scattered light detected to be reduced by two to four orders of magnitude and the contrast between fog and target to be increased significantly. Crucially, this approach delivers robust contrast enhancement regardless of whether the target surface is depolarizing Lambertian or perfectly reflecting. Full article

Heart rate variability (HRV) is a non-invasive marker of cardiac autonomic regulation that reflects the dynamic interaction between sympathetic and parasympathetic influences on the sinoatrial node. Reduced HRV is a hallmark of autonomic dysfunction and has been consistently associated with adverse outcomes across a wide range of cardiovascular conditions, particularly heart failure (HF). HRV is markedly reduced in HF, reflecting profound autonomic imbalance characterized by vagal withdrawal, impaired baroreflex sensitivity, and altered cardiorespiratory coupling. In heart failure with reduced ejection fraction (HFrEF), lower global HRV, particularly reduced SDNN, is consistently associated with mortality, sudden cardiac death, and disease progression. In heart failure with preserved ejection fraction (HFpEF), emerging observational evidence suggests that HRV alterations may accompany early autonomic dysregulation and may be associated with sex-specific patterns, although their mechanistic and prognostic significance remains incompletely defined. In acute HF, HRV assessed during hospitalization may provide additional prognostic information, although current evidence remains limited and heterogeneous. Pharmacological therapies, cardiac resynchronization therapy, exercise training, and lifestyle interventions have variably modulated HRV across studies, but the evidence is heterogeneous and changes in HRV should not be assumed to translate directly into improved clinical outcomes. Despite persistent challenges related to methodological standardization and clinical implementation, emerging technologies and multimodal approaches may refine the feasibility of integrating HRV into risk assessment frameworks. This narrative review aims to summarize the physiological basis of HRV, critically evaluate its alterations across different HF phenotypes, and discuss its prognostic associations, therapeutic modulation, and current practical limitations in clinical application. Full article

Background: Subarachnoid hemorrhage (SAH) induces a sympathetic surge and systemic inflammation that may impair renal perfusion and glomerular integrity. Although the vagus nerve is central to autonomic and anti-inflammatory regulation, its relationship to renal structural injury in severe SAH is unclear. This study evaluated whether electrophysiological vagal CAP amplitude correlates with glomerular integrity in an experimental SAH model. Methods: Nineteen rabbits were assigned to control (n = 5), sham (n = 5), and SAH groups (n = 9). SAH was induced by daily cisterna magna injections of autologous blood for three days, and animals were followed for 14 days; those that did not survive to the 14-day endpoint formed the SAH-Nonsurvivor subgroup (n = 4). Vagal compound action potential (CAP) amplitude (mV) was recorded electrophysiologically and used as the principal physiologic readout of vagal nerve integrity. Renal tissue and perirenal parasympathetic ganglia were analyzed histologically and stereologically to quantify degenerated neurons and atrophic glomeruli (per mm³). Vagal CAP amplitude decreased from 1.42 ± 0.36 mV in controls to 0.34 ± 0.11 mV in the SAH-Nonsurvivor subgroup (p < 0.001), while atrophic glomeruli increased from 4 ± 1 to 98 ± 11 per mm³. Degenerated neuronal density peaked in the SAH-Nonsurvivor subgroup (98 ± 19 per mm³). Vagal CAP amplitude was inversely correlated with glomerular injury (Spearman ρ = −0.89; 95% CI −0.96 to −0.73; p < 0.001). Conclusions: In this small exploratory study, reduced vagal CAP amplitude was associated with greater glomerular injury after severe SAH. These hypothesis-generating findings warrant confirmation in larger, adequately powered studies before any physiologic or translational interpretation can be made. Full article

Urban intelligent transportation systems increasingly rely on vehicle-to-infrastructure (V2I) communication for green-light optimal speed advisory (GLOSA) services. However, conventional GLOSA systems are vulnerable to roadside unit (RSU) coverage gaps and communication instability in mixed-traffic environments. In this paper, we propose a heterogeneous communication network cooperation framework that integrates decentralized multi-hop vehicle-to-vehicle (V2V) relaying with conventional V2I communication to extend signal phase and timing (SPaT) dissemination beyond direct RSU coverage. A lightweight gradient-based speed synchronization mechanism supports real-time trajectory adaptation with low computational overhead. The framework is evaluated through microscopic SUMO simulations with explicit communication impairment modeling across varied traffic densities and connected autonomous vehicle (CAV) penetration levels (10–70%). The results demonstrate reductions in travel time reductions of up to 22%, stop frequency of up to 95%, and CO₂ emission exceeding 18% relative to V2I-only GLOSA under 70% CAV penetration. At the lower bound of 10% CAV penetration, the framework still achieves measurable improvements of approximately 4–6% in travel time and 15–20% in stop frequency, confirming practical benefit even under minimal connected-vehicle adoption. The proposed framework maintains advisory continuity through distributed relay dissemination, offering a scalable and communication-resilient enhancement to intelligent transportation coordination in heterogeneous environments. Full article

Background/Objectives: Long COVID is frequently characterized by neurological, cognitive, neuropsychiatric, and autonomic symptoms (NeuroCOVID). However, their impact on daily functioning remains insufficiently investigated. This study evaluated the association between NeuroCOVID burden and functional impairment among Italian Long COVID survivors. Methods: A secondary cross-sectional analysis was conducted on 250 adults using a validated Italian Long COVID questionnaire. A NeuroCOVID Burden Score (10 symptom domains) and a Functional Impairment Score (daily activities) were constructed and analyzed using correlation and multivariable linear regression. Results: The sample (mean age 33.2 years; 63.6% female) demonstrated high internal consistency for both scores. A strong positive correlation was found between NeuroCOVID burden and functional impairment (r = 0.703; p < 0.001). Conclusions: Persistent NeuroCOVID burden was strongly associated with greater limitations in daily activities. In multivariable regression, NeuroCOVID Burden Score remained independently associated with functional impairment (B = 0.671; 95% CI 0.566–0.776; p < 0.001), together with acute COVID-19 severity (B = 0.156; 95% CI 0.055–0.257; p = 0.003). The final model explained 52.5% of the variance in functional impairment (R² = 0.525). Full article

Electrodermal activity (EDA) has emerged as a promising physiological measure for objectively assessing neurodevelopmental disorders (NDDs) and related disorders, yet its effectiveness across conditions remains unclear. Following PRISMA guidelines, this review analyzed 23 studies (ASD: 11 studies, 410 participants; ADHD: 7 studies, 900 participants; OCD: 5 studies, 154 participants) published between 2010 and 2024 with a focus on methodology, including measurement protocols, signal processing, and analytical approaches. EDA demonstrated utility for diagnostic differentiation, predictive modeling, and physiological evaluation across conditions, with consistent patterns of heightened social arousal in ASD, medication-responsive sympathetic differences in ADHD, and impaired fear extinction in OCD. Machine learning approaches improved performance when combining EDA with multimodal physiological measures. However, substantial methodological heterogeneity existed across devices, recording sites, sampling frequencies, and signal processing, with 11 studies lacking signal processing details and 10 omitting sampling frequencies. The absence of standardized cross-disorder comparisons limited identification of disorder-specific versus shared autonomic signatures. While wearable technologies can enable continuous real-world monitoring, motion artifacts and signal quality remain challenges. Overall, standardized protocols and larger multimodal longitudinal studies are needed to establish EDA as a clinically useful biomarker for disorder assessment and personalized interventions. Full article

Background/Objectives: Long COVID is characterised by persistent symptoms such as fatigue, pain, cognitive impairment, sleep disturbances, and reduced quality of life (QoL) following SARS-CoV-2 infection. Proposed mechanisms include persistent immune activation, chronic inflammation, oxidative stress, endothelial dysfunction, mitochondrial disturbances, and virus-induced cellular senescence. Current management is largely supportive, highlighting the need for complementary strategies targeting these pathways. Natural polyphenols such as quercetin and curcumin possess anti-inflammatory, antioxidant, immunomodulatory, and potential senolytic properties that may modulate multiple pathways implicated in Long COVID. This study aimed to explore the potential complementary effects of oral quercetin–curcumin co-supplementation, administered alongside usual symptomatic management, in adults with persistent Long COVID symptoms. Methods: This single-centre, open-label, single-arm, pragmatic exploratory study enrolled 15 adults with Long COVID in an outpatient real-life clinical practice setting. Participants received a nutraceutical formulation containing quercetin (65 mg) and Curcuma longa extract standardised to provide 42 mg curcumin (Nasafytol^®), administered as two capsules twice daily for 8 weeks in addition to standard care. The primary endpoint was change in overall symptom burden assessed using the COVID-19 Yorkshire Rehabilitation Scale (C19-YRS). Secondary outcomes included fatigue (Fatigue Severity Scale, FSS), pain (Brief Pain Inventory—Short Form, BPI-SF), cognitive function (Patient-Reported Outcomes Measurement Information System Cognitive Function Short Form 8a, PROMIS-CF-8a), mood (Hospital Anxiety and Depression Scale, HADS), sleep quality (Pittsburgh Sleep Quality Index, PSQI), autonomic symptoms (Composite Autonomic Symptom Score-31, COMPASS-31), and health-related QoL (Medical Outcomes Study 36-Item Short-Form Health Survey, SF-36). Results: After 8 weeks, overall symptom burden significantly decreased (C19-YRS median 50 to 32; q = 0.018). Significant reductions were observed in patient-reported fatigue (q = 0.006), pain severity and interference (q = 0.006), and improved physical health-related QoL (SF-36 PCS; q = 0.025). Numerically favourable changes were also observed in cognitive function, anxiety, sleep quality, and autonomic symptoms, although these did not reach statistical significance. The supplementation was generally well tolerated with no serious adverse events. Conclusions: Quercetin–curcumin co-supplementation was associated with lower patient-reported symptom burden, fatigue, and pain and better physical health-related QoL after 8 weeks of supplementation in adults with Long COVID. These observed findings represent treatment-associated changes within this uncontrolled exploratory study and should be interpreted cautiously. Further evaluation in adequately powered randomised placebo-controlled trials is warranted. Trial registration: ClinicalTrials.gov (ID NCT06974058). Full article