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A Noval Load-Dependent Multimodal Vibration Signal Enhancement and Fusion Framework (LD-MVSEFF) for Load-Specific Condition Monitoring
Shahd Ziad Hejazi
,Michael Packianather
Posted: 13 January 2026
The Prognostic Value of Dynamic Changes in Prognostic Nutritional Index (PNI) During Treatment in Lung Cancer: Is Improvement a Better Predictor than Baseline?
Eren Mingsar
,Ilhan öztop
,Sinan Ünal
Posted: 13 January 2026
Celestial and Quantum Dynamics as 4D Relativistic Cloud-Worlds Embedded in a 4D Conformal Bulk: From String to Cloud Theory
Mohammed B. Al-Fadhli
Posted: 13 January 2026
Interhemispheric Functional Hypoconnectivity Is an Early Marker of Cortical Epileptogenesis
Tatiana M Medvedeva
,Lyudmila V Vinogradova
Posted: 13 January 2026
A Technological Blueprint for Smart and AI-Driven Hospitality in Emerging Tourism Markets: Evidence from Albania
Tea Tavanxhiu
,Majlinda Godolja
,Kozeta Sevrani
,Matilda Naco
Posted: 13 January 2026
Lack of Avoidance Behavior in Wind Farms by Young Spanish Imperial Eagles
Angele Alloing
,Roberto Muriel
,Ryan Bambusch
,Jorge García-Macía
,Virginia Morandini
,Miguel Ferrer
Posted: 13 January 2026
Mediterranean Diet Adherence and Vitamin Intake Adequacy in Spanish University Students: Associations with Body Composition and Physical Activity
Cristina Petisco-Rodríguez
,Gema Barrientos-Vicho
,Francisco Javier Alves-Vas
,Ignacio Bartolomé
Posted: 13 January 2026
The G Model: A Geometric Approach to Absolute Data Coherence in Information Systems
José Vicente Quiles Feliu
Posted: 13 January 2026
Isolation of (+)-Catechin from Food Waste Using Ionic Liquids-Modified ZIF67 Covered Silica
Mengshuai Liu
,Xiaoman Li
,Mengmeng Zhao
,Xuyang Jiu
,Chuang Yao
,Minglei Tian
Background: Food waste contains abundant (+)-catechin, but its efficient recovery remains challenging. This study aimed to prepare ionic liquid (IL)-modified sorbents and establish an efficient method for (+)-catechin recovery from chocolate waste via solid-phase extraction (SPE); Methods: Three serious of IL-modified sorbents (Sil-IL, ZIF67-IL, Sil@ZIF67-IL) were synthesized. Their adsorption performance was evaluated under different conditions; adsorption isotherms and kinetics were fitted to Langmuir/Freundlich and pseudo-first/second-order models, respectively. Sorbent stability and (+)-catechin recovery from chocolate waste extracts were tested; Results: Sil@ZIF67-Hmim showed the highest adsorption capacity (154.4 mg/g) at 25 °C within 120 min. Adsorption followed the Langmuir model (R²=0.99), indicating chemical adsorption. Sil@ZIF67-Hmim was subjected to repeated solid phase extraction (SPE) for five consecutive days, the recovery rate ranged from 98.1%-99.2%, and the relative standard deviation (RSD) was 3.2%-4.4%; Conclusion: Sil@ZIF67-Hmim is a high-efficiency sorbent for (+)-catechin recovery from chocolate waste, providing a novel approach for food waste valorization and highlighting the application potential of IL-modified MOF-silica composites.
Background: Food waste contains abundant (+)-catechin, but its efficient recovery remains challenging. This study aimed to prepare ionic liquid (IL)-modified sorbents and establish an efficient method for (+)-catechin recovery from chocolate waste via solid-phase extraction (SPE); Methods: Three serious of IL-modified sorbents (Sil-IL, ZIF67-IL, Sil@ZIF67-IL) were synthesized. Their adsorption performance was evaluated under different conditions; adsorption isotherms and kinetics were fitted to Langmuir/Freundlich and pseudo-first/second-order models, respectively. Sorbent stability and (+)-catechin recovery from chocolate waste extracts were tested; Results: Sil@ZIF67-Hmim showed the highest adsorption capacity (154.4 mg/g) at 25 °C within 120 min. Adsorption followed the Langmuir model (R²=0.99), indicating chemical adsorption. Sil@ZIF67-Hmim was subjected to repeated solid phase extraction (SPE) for five consecutive days, the recovery rate ranged from 98.1%-99.2%, and the relative standard deviation (RSD) was 3.2%-4.4%; Conclusion: Sil@ZIF67-Hmim is a high-efficiency sorbent for (+)-catechin recovery from chocolate waste, providing a novel approach for food waste valorization and highlighting the application potential of IL-modified MOF-silica composites.
Posted: 13 January 2026
Occupational Stress as a Modifiable Risk Factor for Atherosclerotic Coronary Artery Disease: Evidence, Mechanisms, and Interventions
Occupational Stress as a Modifiable Risk Factor for Atherosclerotic Coronary Artery Disease: Evidence, Mechanisms, and Interventions
Dan-Cristian Popescu
,Mara Ciobanu
,Alexandru-Cristian Nechita
Cardiovascular diseases, particularly atherosclerotic coronary artery disease (CAD), remain among the leading causes of mortality worldwide. Although traditional risk factors—such as arterial hypertension, dyslipidemia, diabetes mellitus, obesity, smoking, and physical inactivity—are well established, accumulating evidence highlights the significant role of psychosocial factors in modulating cardiovascular risk. Among these, occupational stress—conceptualized through models such as job strain (high job demands combined with low control) and effort–reward imbalance—has been consistently associated with an increased risk of coronary events. The interaction between occupational stress and classical cardiovascular risk factors remains insufficiently elucidated and challenging to quantify. This review examines the current scientific evidence regarding the relationship between occupational stress and CAD, synthesizing findings from major epidemiological studies and relevant meta-analyses. Chronic exposure to work-related stress activates neuroendocrine pathways, including the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, promotes a state of low-grade systemic inflammation, and facilitates the adoption of unhealthy behaviors such as smoking, poor dietary habits, physical inactivity, and excessive alcohol consumption. These mechanisms contribute to endothelial dysfunction, hypercoagulability, and acceleration of the atherosclerotic process. Landmark investigations, including the INTERHEART study, meta-analyses conducted by Kivimäki and colleagues, and prospective studies by Chandola on the metabolic syndrome, support both the cumulative and independent impact of occupational stress on cardiovascular risk. Although the proportion of risk attributable to occupational stress is lower than that associated with traditional risk factors, its modifiable nature underscores a substantial potential for targeted preventive interventions. Strategies aimed at reducing occupational stress encompass individual-level approaches (stress management programs, lifestyle modification, psychological support), organizational interventions (optimizing the balance between job demands and employee control, enhancing social support in the workplace), and public health policies (occupational health promotion programs, regulatory measures addressing work-related stress, and screening for occupational stress). Recognizing occupational stress as a modifiable risk factor for CAD has important implications for both clinical practice and public health. Future research should focus on large-scale longitudinal studies, the identification of stress-related biomarkers, and the cost-effectiveness of stress-reduction interventions in the prevention and management of coronary artery disease.
Cardiovascular diseases, particularly atherosclerotic coronary artery disease (CAD), remain among the leading causes of mortality worldwide. Although traditional risk factors—such as arterial hypertension, dyslipidemia, diabetes mellitus, obesity, smoking, and physical inactivity—are well established, accumulating evidence highlights the significant role of psychosocial factors in modulating cardiovascular risk. Among these, occupational stress—conceptualized through models such as job strain (high job demands combined with low control) and effort–reward imbalance—has been consistently associated with an increased risk of coronary events. The interaction between occupational stress and classical cardiovascular risk factors remains insufficiently elucidated and challenging to quantify. This review examines the current scientific evidence regarding the relationship between occupational stress and CAD, synthesizing findings from major epidemiological studies and relevant meta-analyses. Chronic exposure to work-related stress activates neuroendocrine pathways, including the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system, promotes a state of low-grade systemic inflammation, and facilitates the adoption of unhealthy behaviors such as smoking, poor dietary habits, physical inactivity, and excessive alcohol consumption. These mechanisms contribute to endothelial dysfunction, hypercoagulability, and acceleration of the atherosclerotic process. Landmark investigations, including the INTERHEART study, meta-analyses conducted by Kivimäki and colleagues, and prospective studies by Chandola on the metabolic syndrome, support both the cumulative and independent impact of occupational stress on cardiovascular risk. Although the proportion of risk attributable to occupational stress is lower than that associated with traditional risk factors, its modifiable nature underscores a substantial potential for targeted preventive interventions. Strategies aimed at reducing occupational stress encompass individual-level approaches (stress management programs, lifestyle modification, psychological support), organizational interventions (optimizing the balance between job demands and employee control, enhancing social support in the workplace), and public health policies (occupational health promotion programs, regulatory measures addressing work-related stress, and screening for occupational stress). Recognizing occupational stress as a modifiable risk factor for CAD has important implications for both clinical practice and public health. Future research should focus on large-scale longitudinal studies, the identification of stress-related biomarkers, and the cost-effectiveness of stress-reduction interventions in the prevention and management of coronary artery disease.
Posted: 13 January 2026
Digital Medicine in the Management of Heart Failure: From 2Reactive Care to Predictive, Pathophysiology-Driven Strategies
Ulvi Mirzoyev
,Kanan Mirzoyev
Background: Heart failure (HF) is a progressive, multisystem syndrome characterized by recurrent decompensation, high hospitalization rates, and substantial mortality. Conventional HF management is mainly episodic and often fails to detect worsening conditions in advanced disease. Digital medicine and remote patient monitoring (RPM) hold promise for moving HF care toward earlier detection, proactive action, and personalized care. Methods: We conduct a narrative review to summarize evidence from randomized clinical trials, real-world registries, and emerging digital health technologies regarding the present and future utility of digital medicine in HF care. There is greater emphasis on pathophysiology-based surveillance, personalized care models, and integration into planned health care pathways. Results: Integrated digital interventions, such as implantable hemodynamic monitoring, organized telemedicine programs, or device-based diagnostic technologies, can minimize HF hospitalizations, prolong life, improve quality of life, and optimize resource utilization in health care systems when incorporated into coordinated care. Crucially, trials emphasize that clinical benefit depends not on technology but on a prompt clinical response, multidisciplinary cooperation, and ongoing interaction between the patient and the doctor. New technologies—including voice-based biomarkers, smartphone-derived photoplethysmography, ballistocardiography, and artificial intelligence–driven data integration—may help transition RPM from a hardware-based system to a scalable, “deviceless” approach. Conclusions: Digital medicine is a game-changer for reimagining HF care, involving not only continuous monitoring of physiological changes but also personalized, proactive clinical decision-making. To implement truly patient-centered, predictive HF management in the years to come, technological innovation must be combined with human connection, ethical governance, and health-system readiness.
Background: Heart failure (HF) is a progressive, multisystem syndrome characterized by recurrent decompensation, high hospitalization rates, and substantial mortality. Conventional HF management is mainly episodic and often fails to detect worsening conditions in advanced disease. Digital medicine and remote patient monitoring (RPM) hold promise for moving HF care toward earlier detection, proactive action, and personalized care. Methods: We conduct a narrative review to summarize evidence from randomized clinical trials, real-world registries, and emerging digital health technologies regarding the present and future utility of digital medicine in HF care. There is greater emphasis on pathophysiology-based surveillance, personalized care models, and integration into planned health care pathways. Results: Integrated digital interventions, such as implantable hemodynamic monitoring, organized telemedicine programs, or device-based diagnostic technologies, can minimize HF hospitalizations, prolong life, improve quality of life, and optimize resource utilization in health care systems when incorporated into coordinated care. Crucially, trials emphasize that clinical benefit depends not on technology but on a prompt clinical response, multidisciplinary cooperation, and ongoing interaction between the patient and the doctor. New technologies—including voice-based biomarkers, smartphone-derived photoplethysmography, ballistocardiography, and artificial intelligence–driven data integration—may help transition RPM from a hardware-based system to a scalable, “deviceless” approach. Conclusions: Digital medicine is a game-changer for reimagining HF care, involving not only continuous monitoring of physiological changes but also personalized, proactive clinical decision-making. To implement truly patient-centered, predictive HF management in the years to come, technological innovation must be combined with human connection, ethical governance, and health-system readiness.
Posted: 13 January 2026
Digital Reconstruction of Hong'an Homespun Using AI and Semantic Differential Method
Tianqing Zhang
,Ce Wang
,Victor Kuzmichev
,Xiaolong Dond
,Lin Xing
Posted: 13 January 2026
FOXC1 Regulates Transcriptional Control of Cytokine Signaling, Selective Inflammatory Pathways and Retinoid Metabolism to Maintain Epithelial Homeostasis, Cell Fate and Integrity in Limbal Epithelial Cells, In Vitro
FOXC1 Regulates Transcriptional Control of Cytokine Signaling, Selective Inflammatory Pathways and Retinoid Metabolism to Maintain Epithelial Homeostasis, Cell Fate and Integrity in Limbal Epithelial Cells, In Vitro
Swarnali Kundu
,Maryam Amini
,Tanja Stachon
,Fabian Fries
,Berthold Seitz
,Zhen Li
,Shuailin Li
,Shanhe Liu
,Shao-Lun Shu
,Shweta Suiwal
+1 authors
This study aimed to evaluate FOXC1-mediated regulatory mechanisms on gene and protein expression profiles in primary human limbal epithelial cells (pLECs), via siRNA knockdown; under basal and lipopolysaccharide (LPS) and interleukin-1β (IL-1β) induced inflammatory conditions. Gene expression was analysed for markers related to inflammation (CCL2, IL-6, IL-8, TNF-α, TGF-β), epithelial differentiation (KRT3, KRT12, KRT13, PAX6, FOXC1), cell proliferation and remodelling (FOSL2, MKi67, MMP2, VEGFA) and retinoic acid metabolism (ALDH3A1, CRABP2, CYP1B1, FABP5, RDH10, RBP1, STRA6). FOXC1 siRNA silencing in human pLECs significantly altered mRNA expression across multiple functional pathways, including inflammatory signaling (CCL2, IL-6, IL-8, IL-1α, VEGFA; p≤0.030), epithelial differentiation (KRT12, KRT13, PAX6; p≤0.045), cell proliferation and stress response (FOSL2, MKi67, VEGFA; p≤0.048) and retinoic acid metabolism (ALDH3A1, CRABP2, CYP1B1, FABP5, RDH10, STRA6; p≤0.037). Corresponding protein levels, evaluated by Western blotting and ELISA, were significantly modulated for the FABP5–CRABP2 axis, IL-6, IL-8, IL-1α, KRT12, KRT13, TGF-β, and RDH10 under different treatment conditions; (p≤0.045). FOXC1 maintains an anti-inflammatory, immune-quiescent state and coordinates TGF-β–mediated signaling, keratin expression, and retinoic acid metabolism to preserve corneal epithelial identity and homeostasis. Disruption of FOXC1 expression perturbs these pathways, potentially predisposing the ocular surface to fibrosis, lineage instability, and impaired regenerative capacity.
This study aimed to evaluate FOXC1-mediated regulatory mechanisms on gene and protein expression profiles in primary human limbal epithelial cells (pLECs), via siRNA knockdown; under basal and lipopolysaccharide (LPS) and interleukin-1β (IL-1β) induced inflammatory conditions. Gene expression was analysed for markers related to inflammation (CCL2, IL-6, IL-8, TNF-α, TGF-β), epithelial differentiation (KRT3, KRT12, KRT13, PAX6, FOXC1), cell proliferation and remodelling (FOSL2, MKi67, MMP2, VEGFA) and retinoic acid metabolism (ALDH3A1, CRABP2, CYP1B1, FABP5, RDH10, RBP1, STRA6). FOXC1 siRNA silencing in human pLECs significantly altered mRNA expression across multiple functional pathways, including inflammatory signaling (CCL2, IL-6, IL-8, IL-1α, VEGFA; p≤0.030), epithelial differentiation (KRT12, KRT13, PAX6; p≤0.045), cell proliferation and stress response (FOSL2, MKi67, VEGFA; p≤0.048) and retinoic acid metabolism (ALDH3A1, CRABP2, CYP1B1, FABP5, RDH10, STRA6; p≤0.037). Corresponding protein levels, evaluated by Western blotting and ELISA, were significantly modulated for the FABP5–CRABP2 axis, IL-6, IL-8, IL-1α, KRT12, KRT13, TGF-β, and RDH10 under different treatment conditions; (p≤0.045). FOXC1 maintains an anti-inflammatory, immune-quiescent state and coordinates TGF-β–mediated signaling, keratin expression, and retinoic acid metabolism to preserve corneal epithelial identity and homeostasis. Disruption of FOXC1 expression perturbs these pathways, potentially predisposing the ocular surface to fibrosis, lineage instability, and impaired regenerative capacity.
Posted: 13 January 2026
Dynamical Exploration of Resting-State Attractors Altered in Major Depressive Disorder
Dynamical Exploration of Resting-State Attractors Altered in Major Depressive Disorder
Leonor Abreu
,Joana Cabral
Major depressive disorder (MDD) represents a heterogeneous condition lacking reliable neurobiological biomarkers and mechanistic understanding. Time-resolved characterisation of brain dynamics reveals that mental health is associated with a characteristic dynamical regime, exhibiting spontaneous switching between a repertoire of ghost attractor states forming resting-state networks. Analysing resting-state fMRI data from 848 MDD patients and 794 healthy controls across 17 sites in China (REST-meta-MDD) using Leading Eigenvector Dynamics Analysis (LEiDA), we found MDD patients exhibit significantly reduced default mode network (DMN) occupancy (p < 0.001; Hedges' g = −0.51) and increased occipito-parieto-temporal state occupancy (p < 0.001; Hedges' g = 0.42), suggesting compensatory dynamical rebalancing. These findings extend prior observations of disrupted DMN in MDD, aligning with the emerging dynamical systems framework for mental health to advance mechanistic understanding of MDD pathophysiology.
Major depressive disorder (MDD) represents a heterogeneous condition lacking reliable neurobiological biomarkers and mechanistic understanding. Time-resolved characterisation of brain dynamics reveals that mental health is associated with a characteristic dynamical regime, exhibiting spontaneous switching between a repertoire of ghost attractor states forming resting-state networks. Analysing resting-state fMRI data from 848 MDD patients and 794 healthy controls across 17 sites in China (REST-meta-MDD) using Leading Eigenvector Dynamics Analysis (LEiDA), we found MDD patients exhibit significantly reduced default mode network (DMN) occupancy (p < 0.001; Hedges' g = −0.51) and increased occipito-parieto-temporal state occupancy (p < 0.001; Hedges' g = 0.42), suggesting compensatory dynamical rebalancing. These findings extend prior observations of disrupted DMN in MDD, aligning with the emerging dynamical systems framework for mental health to advance mechanistic understanding of MDD pathophysiology.
Posted: 13 January 2026
Deep Learning Versus Classical Machine Learning for Schizophrenia Detection from EEG: A Cross-Dataset Generalization Study
Samiksha B. C.
,Eric Raymond
,Divyashree Santosh
,Dana Vrajitoru
,Liqiang Zhang
,Lucas Carpenter
,Tatsiana Krauchonak
,Tika Puri
,Dipak Chaulagain
Posted: 13 January 2026
Metal–Ligand Catalyzed Upgrading of Waste Polyethylene for Industrial Applications
Adetutu Oluwakemi Aliyu
,Olaide Olalekan Wahab
,Abdulafeez Olayinka Akorede
Posted: 13 January 2026
High-Efficiency Neural-Symbolic Framework for Automated Soliton Solutions in (3+1)dimension Fluid Dynamics
Jianglong Shen
,Jingwen Huang
,Baoying Du
,Yuanhua Meng
Posted: 13 January 2026
Association of IL7 rs16906115 Polymorphism with Adverse Events in Patients with Advanced Lung Cancer Undergoing Immunotherapy
Andrea González-Hernández
,Guillermo Paz-López
,Beatriz Martínez-Gálvez
,Felipe Vaca Paniagua
,Isabel Barragán
,Elisabeth Pérez-Ruiz
,Jose Carlos Benitez
,Antonio Rueda-Dominguez
,Javier Oliver
Posted: 13 January 2026
From Subjective to Objective: Validating Patient Satisfaction in Facial Surgery Through Psychometrics
Maarten J. Ottenhof
Posted: 13 January 2026
Revisiting Bill Lands’ Hypotheses: Mechanistic Competition, Immunological and Metabolic Regulation, Unresolved Questions
Ulrich Suchner
The optimal dietary balance between n‑6 and n‑3 polyunsaturated fatty acids (PUFAs), the safe upper intake of n‑6 PUFAs—particularly linoleic acid—and the physiological consequences of their metabolic competition remain unresolved in the context of the Western diet. Since the 1980s, Bill Lands and colleagues have argued that high n‑6 PUFA intake can shift the balance of n‑3–derived pathways and eicosanoid signaling, potentially influencing processes relevant to non‑communicable diseases. Despite its potential public‑health implications, this hypothesis has received limited systematic attention. In this narrative review, we synthesize key aspects of Lands’ work, evaluate supportive and contradictory evidence, and highlight mechanistic insights into lipid competition and inflammatory regulation. We conclude that these unresolved but testable hypotheses warrant renewed investigation, as their corroboration could reshape dietary guidelines and strategies for chronic disease prevention.
The optimal dietary balance between n‑6 and n‑3 polyunsaturated fatty acids (PUFAs), the safe upper intake of n‑6 PUFAs—particularly linoleic acid—and the physiological consequences of their metabolic competition remain unresolved in the context of the Western diet. Since the 1980s, Bill Lands and colleagues have argued that high n‑6 PUFA intake can shift the balance of n‑3–derived pathways and eicosanoid signaling, potentially influencing processes relevant to non‑communicable diseases. Despite its potential public‑health implications, this hypothesis has received limited systematic attention. In this narrative review, we synthesize key aspects of Lands’ work, evaluate supportive and contradictory evidence, and highlight mechanistic insights into lipid competition and inflammatory regulation. We conclude that these unresolved but testable hypotheses warrant renewed investigation, as their corroboration could reshape dietary guidelines and strategies for chronic disease prevention.
Posted: 13 January 2026
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