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29 pages, 1550 KiB  
Review
Phytochemical Modulators of Nociception: A Review of Cannabis Terpenes in Chronic Pain Syndromes
by Aniello Alfieri, Sveva Di Franco, Vincenzo Maffei, Pasquale Sansone, Maria Caterina Pace, Maria Beatrice Passavanti and Marco Fiore
Pharmaceuticals 2025, 18(8), 1100; https://doi.org/10.3390/ph18081100 - 24 Jul 2025
Abstract
Cannabis sativa L. is a phytochemically rich plant with therapeutic potential across various clinical domains, including pain, inflammation, and neurological disorders. Among its constituents, terpenes are gaining recognition for their capacity to modulate the pathophysiological processes underlying chronic pain syndromes. Traditionally valued for [...] Read more.
Cannabis sativa L. is a phytochemically rich plant with therapeutic potential across various clinical domains, including pain, inflammation, and neurological disorders. Among its constituents, terpenes are gaining recognition for their capacity to modulate the pathophysiological processes underlying chronic pain syndromes. Traditionally valued for their aromatic qualities, terpenes such as myrcene, β-caryophyllene (BCP), limonene, pinene, linalool, and humulene have demonstrated a broad spectrum of biological activities. Beyond their observable analgesic, anti-inflammatory, and anxiolytic outcomes, these compounds exert their actions through distinct molecular mechanisms. These include the activation of cannabinoid receptor type 2 (CB2), the modulation of transient receptor potential (TRP) and adenosine receptors, and the inhibition of pro-inflammatory signalling pathways such as Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Cyclooxygenase-2 (COX-2). This narrative review synthesizes the current preclinical and emerging clinical data on terpene-mediated analgesia, highlighting both monoterpenes and sesquiterpenes, and discusses their potential for synergistic interaction with cannabinoids, the so-called entourage effect. Although preclinical findings are promising, clinical translation is limited by methodological variability, the lack of standardized formulations, and insufficient pharmacokinetic characterization. Further human studies are essential to clarify their therapeutic potential. Full article
(This article belongs to the Section Pharmacology)
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16 pages, 2379 KiB  
Article
Atractylodes lancea (Thunb.) DC. [Asteraceae] Rhizome-Derived Exosome-like Nanoparticles Suppress Lipopolysaccharide-Induced Inflammation by Reducing Toll-like Receptor 4 Expression in BV-2 Murine Microglial Cells
by Mizusa Hyodo, Kei Kawada, Tomoaki Ishida, Yuki Izawa-Ishizawa, Ryoko Matoba, Rina Okamoto, Kohei Jobu, Io Horikawa, Fuka Aizawa, Kenta Yagi, Takahiro Niimura, Yayoi Kawano, Shinji Abe, Yukihiro Hamada, Mitsuhiro Goda and Keisuke Ishizawa
Pharmaceuticals 2025, 18(8), 1099; https://doi.org/10.3390/ph18081099 - 24 Jul 2025
Abstract
Background/Objectives: Atractylodes lancea (Thunb.) DC. [Asteraceae] (ALR)-derived exosome-like nanoparticles (ALR-ELNs) exhibit anti-neuroinflammatory effects in microglial cells. However, the associated mechanisms and pathways are unknown. We aimed to characterize the effects of ALR-ELNs on inflammatory responses of BV-2 microglial cells to lipopolysaccharide (LPS) [...] Read more.
Background/Objectives: Atractylodes lancea (Thunb.) DC. [Asteraceae] (ALR)-derived exosome-like nanoparticles (ALR-ELNs) exhibit anti-neuroinflammatory effects in microglial cells. However, the associated mechanisms and pathways are unknown. We aimed to characterize the effects of ALR-ELNs on inflammatory responses of BV-2 microglial cells to lipopolysaccharide (LPS) using RNA sequencing. Methods: ALR-ELNs were fractionated from ALR. BV-2 microglial murine cells were stimulated with LPS after treatment with ALR-ELNs. RNA sequencing was performed to analyze variations in mRNA levels. Ingenuity pathway analysis (IPA) was performed to investigate the mechanism of action of ALR-ELNs. mRNA expression was assessed using real-time quantitative polymerase chain reaction (qPCR). Results: The expression of 651 genes was downregulated, whereas that of 1204 genes was upregulated in LPS-stimulated BV2 cells pretreated with ALR-ELNs. The IPA showed that the effects of ALR-ELNs on inflammation took place through pathogen-influenced signaling. Network analysis via IPA showed that the Toll-like receptor (TLR) is involved in the suppression of inflammation by ALR-ELNs. The qPCR analysis showed that pretreatment with ALR-ELNs significantly reduced TLR4 mRNA expression. Conclusions: ALR-ELNs suppress the release of inflammatory mediators by downregulating TLR4 expression, which is a novel mechanism by which ALR-ELNs act on microglia. Identifying active ingredients in ALR-ELNs that downregulate TLR4 expression can advance the development of therapeutic drugs for neuroinflammatory diseases. Full article
(This article belongs to the Section Natural Products)
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29 pages, 1209 KiB  
Review
The Oral–Gut Microbiota Axis as a Mediator of Frailty and Sarcopenia
by Domenico Azzolino, Margherita Carnevale-Schianca, Lucrezia Bottalico, Marica Colella, Alessia Felicetti, Simone Perna, Leonardo Terranova, Franklin Garcia-Godoy, Mariangela Rondanelli, Pier Carmine Passarelli and Tiziano Lucchi
Nutrients 2025, 17(15), 2408; https://doi.org/10.3390/nu17152408 - 23 Jul 2025
Viewed by 44
Abstract
Traditionally studied in isolation, the oral and gut microbiota are now being recognized as interconnected through anatomical and physiological pathways forming a dynamic “oral–gut microbiota axis”. Both oral and gut microbiota undergo changes with aging, characterized by a decline in microbial diversity and [...] Read more.
Traditionally studied in isolation, the oral and gut microbiota are now being recognized as interconnected through anatomical and physiological pathways forming a dynamic “oral–gut microbiota axis”. Both oral and gut microbiota undergo changes with aging, characterized by a decline in microbial diversity and a shift toward potentially harmful species. The aim of this review is, therefore, to provide an overview of oral–gut communications in mediating frailty and sarcopenia. PubMed, EMBASE and Scopus databases were searched for relevant articles. We limited our search to manuscripts published in the English language. Interactions between oral and gut microbiota occur mainly through three pathways namely the enteral, the bloodstream and the fecal-oral routes. Alterations in the oral–gut microbiota axis contribute to chronic low-grade inflammation (i.e., “inflamm-ageing”) and mitochondrial dysfunction, key mechanisms underlying frailty and sarcopenia. Microbial metabolites, such as short-chain fatty acids and modified bile acids, appear to play an emerging role in influencing microbial homeostasis and muscle metabolism. Furthermore, poor oral health associated with microbial dysbiosis may contribute to altered eating patterns that negatively impact gut microbiota eubiosis, further exacerbating muscle decline and the degree of frailty. Strategies aimed at modulating the microbiota, such as healthy dietary patterns with reduced consumption of ultra-processed foods, refined carbohydrates and alcohol, ensuring an adequate protein intake combined with physical exercise, as well as supplementation with prebiotics, probiotics, and omega-3 polyunsaturated fatty acids, are increasingly recognized as promising interventions to improve both oral and gut microbiota health, with beneficial effects on frailty and sarcopenia. A better understanding of the oral–gut microbiota axis offers promising insights into nutritional interventions and therapeutic strategies for the age-related muscle decline, frailty and systemic health maintenance. Full article
(This article belongs to the Special Issue Addressing Malnutrition in the Aging Population)
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18 pages, 454 KiB  
Article
How Knowledge Management Capability Drives Sustainable Business Model Innovation: A Combination of Symmetric and Asymmetric Approaches
by Shuting Chen, Liping Huang and Aojie Zhou
Sustainability 2025, 17(15), 6714; https://doi.org/10.3390/su17156714 - 23 Jul 2025
Viewed by 38
Abstract
In a business environment with rapidly growing digital technologies, knowledge management (KM) capability is an indispensable source for enterprise innovation activities. Nevertheless, there is limited understanding of the specific KM capability that leads to sustainable business model innovation (SBMI). This study therefore aimed [...] Read more.
In a business environment with rapidly growing digital technologies, knowledge management (KM) capability is an indispensable source for enterprise innovation activities. Nevertheless, there is limited understanding of the specific KM capability that leads to sustainable business model innovation (SBMI). This study therefore aimed to investigate the internal relationship between KM capability and SBMI by leveraging dynamic capability theory. A hierarchical regression analysis (HRA) and a fuzzy set qualitative comparative analysis (fsQCA) are used to analyze a sample of 115 Chinese innovative enterprises. The results indicate that organizational structure promotes information technology by improving human capital, and that information technology then stimulates collaboration depth by expanding collaboration breadth, thereby driving SBMI. Specifically, human capital, information technology, collaboration breadth, and collaboration depth play significant chain-mediating roles in the relationship between organizational structure and SBMI. This study contributes to the literature on KM and innovation management, extends the use of low-order and high-order dynamic capabilities in DCT, and assists managers in developing SBMI effectively. Full article
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30 pages, 470 KiB  
Article
Digital Intelligence and Decision Optimization in Healthcare Supply Chain Management: The Mediating Roles of Innovation Capability and Supply Chain Resilience
by Jing-Yan Ma and Tae-Won Kang
Sustainability 2025, 17(15), 6706; https://doi.org/10.3390/su17156706 - 23 Jul 2025
Viewed by 52
Abstract
Healthcare supply chain management operates amid fluctuating patient demand, rapidly advancing biotechnologies, and unpredictable supply disruptions pose high risks and create an imperative for sustainable resource optimization. This study investigates the underlying mechanisms through which digital intelligence drives strategic decision optimization in healthcare [...] Read more.
Healthcare supply chain management operates amid fluctuating patient demand, rapidly advancing biotechnologies, and unpredictable supply disruptions pose high risks and create an imperative for sustainable resource optimization. This study investigates the underlying mechanisms through which digital intelligence drives strategic decision optimization in healthcare supply chains. Drawing on the Resource-Based View and Dynamic Capabilities Theory, we develop a chain-mediated model, defined as the multistage indirect path whereby digital intelligence first bolsters innovation capability, which then activates supply chain resilience (absorptive, response, and restorative capability), to improve decision optimization. Data were collected from 360 managerial-level respondents working in healthcare supply chain organizations in China, and the proposed model was tested using structural equation modeling. The results indicate that digital intelligence enhances innovation capability, which in turn activates all three dimensions of resilience, producing a synergistic effect that promotes sustained decision optimization. However, the direct effect of digital intelligence on decision optimization was not statistically significant, suggesting that its impact is primarily mediated through organizational capabilities, particularly supply chain resilience. Practically, the findings suggest that in the process of deploying digital intelligence systems and platforms, healthcare organizations should embed technological advantages into organizational processes, emergency response mechanisms, and collaborative operations, so that digitalization moves beyond the technical system level and is truly internalized as organizational innovation capability and resilience, thereby leading to sustained improvement in decision-making performance. Full article
(This article belongs to the Section Sustainable Management)
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28 pages, 5780 KiB  
Article
Multiscale Modeling and Dynamic Mutational Profiling of Binding Energetics and Immune Escape for Class I Antibodies with SARS-CoV-2 Spike Protein: Dissecting Mechanisms of High Resistance to Viral Escape Against Emerging Variants
by Mohammed Alshahrani, Vedant Parikh, Brandon Foley and Gennady Verkhivker
Viruses 2025, 17(8), 1029; https://doi.org/10.3390/v17081029 - 23 Jul 2025
Viewed by 52
Abstract
The rapid evolution of SARS-CoV-2 has underscored the need for a detailed understanding of antibody binding mechanisms to combat immune evasion by emerging variants. In this study, we investigated the interactions between Class I neutralizing antibodies—BD55-1205, BD-604, OMI-42, P5S-1H1, and P5S-2B10—and the receptor-binding [...] Read more.
The rapid evolution of SARS-CoV-2 has underscored the need for a detailed understanding of antibody binding mechanisms to combat immune evasion by emerging variants. In this study, we investigated the interactions between Class I neutralizing antibodies—BD55-1205, BD-604, OMI-42, P5S-1H1, and P5S-2B10—and the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein using multiscale modeling, which combined molecular simulations with the ensemble-based mutational scanning of the binding interfaces and binding free energy computations. A central theme emerging from this work is that the unique binding strength and resilience to immune escape of the BD55-1205 antibody are determined by leveraging a broad epitope footprint and distributed hotspot architecture, additionally supported by backbone-mediated specific interactions, which are less sensitive to amino acid substitutions and together enable exceptional tolerance to mutational escape. In contrast, BD-604 and OMI-42 exhibit localized binding modes with strong dependence on side-chain interactions, rendering them particularly vulnerable to escape mutations at K417N, L455M, F456L and A475V. Similarly, P5S-1H1 and P5S-2B10 display intermediate behavior—effective in some contexts but increasingly susceptible to antigenic drift due to narrower epitope coverage and concentrated hotspots. Our computational predictions show strong agreement with experimental deep mutational scanning data, validating the accuracy of the models and reinforcing the value of binding hotspot mapping in predicting antibody vulnerability. This work highlights that neutralization breadth and durability are not solely dictated by epitope location, but also by how binding energy is distributed across the interface. The results provide atomistic insight into mechanisms driving resilience to immune escape for broadly neutralizing antibodies targeting the ACE2 binding interface—which stems from cumulative effects of structural diversity in binding contacts, redundancy in interaction patterns and reduced vulnerability to mutation-prone positions. Full article
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31 pages, 4221 KiB  
Article
Estradiol Downregulates MicroRNA-193a to Mediate Its Angiogenic Actions
by Lisa Rigassi, Mirel Adrian Popa, Ruth Stiller, Brigitte Leeners, Marinella Rosselli and Raghvendra Krishna Dubey
Cells 2025, 14(15), 1134; https://doi.org/10.3390/cells14151134 - 23 Jul 2025
Viewed by 128
Abstract
Estrogens regulate many physiological processes in the human body, including the cardiovascular system. Importantly, Estradiol (E2) exerts its vascular protective actions, in part, by promoting endothelial repair via induction of endothelial cell (EC) proliferation, migration and angiogenesis. Recent evidence that microRNAs (miRNAs) play [...] Read more.
Estrogens regulate many physiological processes in the human body, including the cardiovascular system. Importantly, Estradiol (E2) exerts its vascular protective actions, in part, by promoting endothelial repair via induction of endothelial cell (EC) proliferation, migration and angiogenesis. Recent evidence that microRNAs (miRNAs) play an important role in vascular health and disease as well as in regulating Estrogen actions in many cell types. We hypothesize that E2 may mediate its vascular protective actions via the regulation of miRNAs. Following initial screening, we found that E2 downregulates the levels of miR-193a-3p in ECs. Moreover, miR-193a-3p downregulation by miR-193a-3p-antimir mimicked the effects as E2 on EC growth, migration, and capillary formation. Restoring miR-193a-3p levels with mimics after E2 treatment abrogated the vasculogenic actions of E2, suggesting a key role of miR-193a-3p in E2-mediated EC-growth-promoting effects. We further investigated the cellular mechanisms involved and found that miR-193a-3p inhibits angiogenesis by blocking phosphoinositide-3-kinase (PI3K)/Akt-vascular endothelial growth factor (VEGF) and Activin receptor-like kinase 1 (ALK1)/SMAD1/5/8 signaling in ECs, both pathways that are important in E2-mediated vascular protection. Additionally, using reverse transcription polymerase chain reaction (RT-PCR), we demonstrate that E2 downregulates miR-193a-3p in ECs via Estrogen Receptor (ER)α, but not ERβ or G protein-coupled estrogen receptor (GPER). Moreover, these actions occur post-transcriptionally, as the expression of pri-miR-193a-3p was not affected. The anti-angiogenic actions of miR-193a-3p were also observed in in vivo Matrigel implant-based capillary formation studies in ovariectomized mice where E2 induced capillary formation, and these effects were abrogated in the presence of miR-193a-3p, but not in the control mimic. Assessment of miR-193a-3p levels in plasma collected from in vitro fertilization (IVF) subjects with low and high E2 levels showed significantly lower miR-193a-3p levels in responders during the high E2 period. Hence, our findings provide the first evidence that miR-193a-3p mimic inhibits angiogenesis whereas its antimir is angiogenic. Importantly, E2 mediates its regenerative actions on ECs/capillary formation by downregulating endogenous miR-193a-3p expression. Both miR-193a-3p mimic or antimir may represent important therapeutic molecules to prevent or to induce endothelial function in treating pathophysiologies associated with capillary growth. Full article
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23 pages, 2056 KiB  
Article
Nanoceria Coated with Maltodextrin or Chitosan: Effects on Key Genes of Oxidative Metabolism, Proliferation, and Autophagy in Human Embryonic Lung Fibroblasts
by Elena V. Proskurnina, Madina M. Sozarukova, Elizaveta S. Ershova, Ekaterina A. Savinova, Larisa V. Kameneva, Natalia N. Veiko, Vladimir P. Saprykin, Khamzat K. Vyshegurov, Vladimir K. Ivanov and Svetlana V. Kostyuk
Molecules 2025, 30(15), 3078; https://doi.org/10.3390/molecules30153078 - 23 Jul 2025
Viewed by 122
Abstract
Nanoceria is a multifaceted enzyme-like catalyst of ROS-mediated (reactive oxygen species) reactions, which results in its multiple biomedical applications. Biodegradable polysaccharide coatings improve biocompatibility, while the effects of these coatings on the ROS-related activity of nanoceria in cells need thorough studies. Here, we [...] Read more.
Nanoceria is a multifaceted enzyme-like catalyst of ROS-mediated (reactive oxygen species) reactions, which results in its multiple biomedical applications. Biodegradable polysaccharide coatings improve biocompatibility, while the effects of these coatings on the ROS-related activity of nanoceria in cells need thorough studies. Here, we used human embryonic lung fibroblasts to study the effects of maltodextrin and chitosan coatings on cellular oxidative metabolism of nanoceria by examining cell viability, mitochondrial potential, accumulation of nanoparticles in cells, intracellular ROS, expression of NOX4 (NADPH oxidase 4), NRF2 (nuclear factor erythroid 2-related factor 2), NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), and STAT3 (signal transducer and activator of transcription 3) proteins as well as the expression of biomarkers of DNA damage/repair, cell proliferation, and autophagy. Both types of polysaccharide-coated nanoceria were non-toxic up to millimolar concentrations. For maltodextrin-coated nano-CeO2, in contrast to bare nanoparticles, there was no oxidative DNA damage/repair with moderate activation of NOX4 expression. Like bare nanoceria, maltodextrin-coated nanoparticles demonstrate the proliferative impact and do not activate autophagy. However, maltodextrin-coated nanoparticles have an activating impact on mitochondrial potential and the NF-κB pathway. Chitosan-coated nanoceria causes short-term intracellular oxidative stress, activation of the expression of NOX4, STAT3, and NRF2, oxidative DNA damage, and double-strand breaks accompanied by activation of DNA repair systems. In contrast to maltodextrin-coated nanoparticles, chitosan-coated nanoceria inhibits the NF-κB pathway and activates autophagy. These findings would be useful in the development of advanced nanoceria-based pharmaceuticals and contribute to the understanding of the biochemical properties of nanoceria as a modulator of ROS-dependent signaling pathways. Full article
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28 pages, 1763 KiB  
Review
Interaction Between Konjac Glucomannan and Gut Microbiota and Its Impact on Health
by Yufen Yu, Shuo Jin, Yi Yang, Xiaodong Han, Rongfa Guan and Hao Zhong
Biology 2025, 14(8), 923; https://doi.org/10.3390/biology14080923 - 23 Jul 2025
Viewed by 51
Abstract
Konjac glucomannan (KGM) is a natural polysaccharide polymer. It is degraded by gut microbiota-derived β-mannanase into small-molecule nutrients, which exert diverse physiological regulatory effects. As a prebiotic, KGM modulates gut microbiota composition. It selectively fosters the proliferation of beneficial commensals and suppresses potential [...] Read more.
Konjac glucomannan (KGM) is a natural polysaccharide polymer. It is degraded by gut microbiota-derived β-mannanase into small-molecule nutrients, which exert diverse physiological regulatory effects. As a prebiotic, KGM modulates gut microbiota composition. It selectively fosters the proliferation of beneficial commensals and suppresses potential pathogens, thereby alleviating microbiota-related disorders. Moreover, microbiota fermentation of KGM produces metabolites. Short-chain fatty acids (SCFAs) are particularly notable among these metabolites. They exert multifaceted beneficial effects, including metabolic regulation, intestinal barrier strengthening, and neuroprotective functions. These effects are mediated through inhibition of inflammatory pathways (e.g., NF-κB, MAPK), modulation of lipid metabolism genes (e.g., CD36), and regulation of neurotransmitters (e.g., GABA, 5-HT). This highlights KGM’s therapeutic potential for metabolic, inflammatory, and neurodegenerative diseases. Current clinical use is limited by dose-dependent adverse effects and interindividual response variability, which stem from different microbial communities. This necessitates personalized dosage strategies. Despite these limitations, KGM as a prebiotic polysaccharide exhibits multifaceted bioactivity. Current evidence suggests its potential to synergistically modulate metabolic pathways, gut microbiota composition, immune cell signaling, and neuroendocrine interactions. This highlights its promise for developing novel therapeutic interventions. Full article
(This article belongs to the Special Issue Gut Microbiome in Health and Disease (2nd Edition))
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23 pages, 39698 KiB  
Article
Anti-C1q Autoantibody-Binding Engineered scFv C1q-Mimicking Fragment Enhances Disease Progression in Lupus-Prone MRL/lpr Mice
by Silviya Bradyanova, Nikolina Mihaylova, Nikola Ralchev, Alexandra Kapogianni, Ginka Cholakova, Kalina Nikolova-Ganeva, Ivanka Tsacheva and Andrey Tchorbanov
Int. J. Mol. Sci. 2025, 26(15), 7048; https://doi.org/10.3390/ijms26157048 - 22 Jul 2025
Viewed by 81
Abstract
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease characterized by tissue damage in multiple organs caused by autoantibodies and the resulting immune complexes. One possible way for complement system contribution to onset of autoimmune disorder could be realized by the impairment [...] Read more.
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease characterized by tissue damage in multiple organs caused by autoantibodies and the resulting immune complexes. One possible way for complement system contribution to onset of autoimmune disorder could be realized by the impairment of C1q-mediated apoptotic clearance as part of human homeostasis. The capacity of C1q to bind early apoptotic cells could be decreased or even lost in the presence of anti-C1q antibodies. A monoclonal anti-idiotypic single-chain (scFv) antibody was selected from the phage library Griffin1” to recognize anti-C1q autoantibodies, purified from sera of lupus nephritis patients. Lupus-prone MRL/lpr mice were injected weekly with scFv A1 fragment-binding anti-C1q antibodies. The number of in vitro and ex vivo studies with collected cells, sera, and organs from the treated animals was performed. scFv treatment changed the percentage of different B-, T-, and NK-cell subpopulations as well as plasma cells and plasmablasts in the spleen and bone marrow. An increase in the levels of splenocyte proliferation, anti-C1q antibodies, and the number of plasma cells producing anti-dsDNA and anti-C1q antibodies were also observed in scFv-treated animals. High levels of proteinuria and hematuria combined with unstable levels of IL10 and IFNγ promote the development of severe lupus and shorten the survival of treated MRL/lpr mice. Therapy with the scFv A1 antibody resulted in BCR recognition on the surface of anti-C1q-specific B-cells and had a disease progression effect, enhancing lupus symptoms in the MRL/lpr mouse model of SLE. Full article
(This article belongs to the Section Molecular Biology)
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17 pages, 6805 KiB  
Article
Ferritin Nanocages Exhibit Unique Structural Dynamics When Displaying Surface Protein
by Monikaben Padariya, Natalia Marek-Trzonkowska and Umesh Kalathiya
Int. J. Mol. Sci. 2025, 26(15), 7047; https://doi.org/10.3390/ijms26157047 - 22 Jul 2025
Viewed by 80
Abstract
Ferritin nanocages with spherical shells carry proteins or antigens that enable their use as highly efficient nanoreactors and nanocarriers. Mimicking the surface Spike (S) receptor-binding domain (RBD) from SARS-CoV-2, ferritin nanocages induce neutralizing antibody production or block viral entry. Herein, by implementing molecular [...] Read more.
Ferritin nanocages with spherical shells carry proteins or antigens that enable their use as highly efficient nanoreactors and nanocarriers. Mimicking the surface Spike (S) receptor-binding domain (RBD) from SARS-CoV-2, ferritin nanocages induce neutralizing antibody production or block viral entry. Herein, by implementing molecular dynamics simulation, we evaluate the efficiency in the interaction pattern (active or alternative sites) of H-ferritin displaying the 24 S RBDs with host-cell-receptor or monoclonal antibodies (mAbs; B38 or VVH-72). Our constructed nanocage targeted the receptor- or antibody-binding interfaces, suggesting that mAbs demonstrate an enhanced binding affinity with the RBD, with key interactions originating from its variable heavy chain. The S RBD interactions with ACE2 and B38 involved the same binding site but led to divergent dynamic responses. In particular, both B38 chains showed that asymmetric fluctuations had a major effect on their engagement with the Spike RBD. Although the receptor increased the binding affinity of VVH-72 for the RBD, the mAb structural orientation on the nanocage remained identical to its conformation when bound to the host receptor. Overall, our findings characterize the essential pharmacophore formed by Spike RBD residues over nanocage molecules, which mediates high-affinity interactions with either binding partner. Importantly, the ferritin-displayed RBD maintained native receptor and antibody binding profiles, positioning it as a promising scaffold for pre-fusion stabilization and protective RBD vaccine design. Full article
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20 pages, 2383 KiB  
Article
Time Perspective and Health Behaviors in Chronic Disease Patients: A Chain Mediation Model of Illness Perception via Temporal Self-Regulation Theory
by Xiaorong Lang, Sufang Huang and Yaru Xiao
Behav. Sci. 2025, 15(8), 996; https://doi.org/10.3390/bs15080996 - 22 Jul 2025
Viewed by 187
Abstract
(1) The formation pathways and underlying mechanisms of health behaviors among young and middle-aged adults with chronic diseases under a temporal perspective remain underexplored. Based on Temporal Self-Regulation Theory and its subsequent extensions, this study aimed to investigate the time perspective among Chinese [...] Read more.
(1) The formation pathways and underlying mechanisms of health behaviors among young and middle-aged adults with chronic diseases under a temporal perspective remain underexplored. Based on Temporal Self-Regulation Theory and its subsequent extensions, this study aimed to investigate the time perspective among Chinese young and middle-aged adults with chronic diseases and analyzed the relationships between time perspective, illness perception, health behavior motivation, and health behaviors, thereby providing valuable empirical evidence for health behavior modification in this population. (2) This study was a cross-sectional survey conducted from March to April 2025. Structural Equation Modeling was employed to investigate the relationships among the variables. (3) This study enrolled a total of 391 participants with high levels of future and past-positive perspectives. Time perspective, directly related to health behaviors, namely past-negative, present-impulsive, and present-fatalistic perspectives, exerted negative associations with health behaviors, respectively, whereas future and past-positive perspectives showed positive associations with health behavior. Analysis of the mediating effect found that illness perception served as a mediator between the time perspective of past-negative, present-impulsive, and present-fatalistic perspectives, and health behaviors. And health behavior motivation acted as a mediator in the relationship between past-negative, present-impulsive, and past-positive perspectives, and health behaviors. Furthermore, illness perception and health behavior motivation formed a chain mediation pathway between time perspective and health behaviors. (4) Time perspective was associated with health behaviors, not only exerting directed effects but also manifesting a double-edged sword effect through illness perception and health behavior motivation. Subsequent interventions targeting health behaviors among young and middle-aged populations in China should incorporate considerations of the temporal perspective’s uniqueness and its intricate mechanisms of action on health behaviors. Full article
(This article belongs to the Special Issue The Role of Future Time Perspective Among Young Adults)
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22 pages, 535 KiB  
Article
Digital Transformation Capability, Organizational Strategic Intuition, and Digital Leadership: Empirical Evidence from High-Tech Firms’ Performance in the Yangtze River Delta
by Yu Zhang, Trairong Swatdikun, Pankaewta Lakkanawanit, Shi-Zheng Huang and Heng Chen
J. Risk Financial Manag. 2025, 18(7), 405; https://doi.org/10.3390/jrfm18070405 - 21 Jul 2025
Viewed by 383
Abstract
Despite growing scholarly interest in digital transformation, few studies have systematically explored the mechanisms linking digital transformation capability to firm performance. This study examines both the direct and indirect effects of digital transformation capability on firm performance, offering novel insights by incorporating organizational [...] Read more.
Despite growing scholarly interest in digital transformation, few studies have systematically explored the mechanisms linking digital transformation capability to firm performance. This study examines both the direct and indirect effects of digital transformation capability on firm performance, offering novel insights by incorporating organizational strategic intuition and digital leadership as mediating variables. These mediators align with the emerging emphasis on strategic risk management in the literature. A survey was conducted among 620 high-tech enterprises in the Yangtze River Delta using a structured questionnaire. The data were analyzed using SPSS 23.0 for descriptive and correlational statistics, SmartPLS 4.0 for structural equation modeling (SEM), and PROCESS 4.2 for mediation analysis. The results reveal a significant direct effect of digital transformation capability on firm performance. Mediation analysis further shows that organizational strategic intuition and digital leadership each significantly mediate this relationship, and a chain mediation pathway involving both variables is also confirmed. These findings deepen our understanding of how digital transformation capability drives performance outcomes and offer practical guidance for high-tech firms seeking sustainable competitive advantages in dynamic digital environments. This study advances the theoretical discourse by clarifying the pathways through which digital transformation capability affects firm performance and provides empirical evidence to inform strategic decision-making in high-tech management. Full article
(This article belongs to the Special Issue The Role of Digitization in Corporate Finance)
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20 pages, 7353 KiB  
Article
Comparative Analysis of Robust Entanglement Generation in Engineered XX Spin Chains
by Eduardo K. Soares, Gentil D. de Moraes Neto and Fabiano M. Andrade
Entropy 2025, 27(7), 764; https://doi.org/10.3390/e27070764 - 18 Jul 2025
Viewed by 169
Abstract
We present a numerical investigation comparing two entanglement generation protocols in finite XX spin chains with varying spin magnitudes (s=1/2,1,3/2). Protocol 1 (P1) relies on staggered couplings to steer correlations toward [...] Read more.
We present a numerical investigation comparing two entanglement generation protocols in finite XX spin chains with varying spin magnitudes (s=1/2,1,3/2). Protocol 1 (P1) relies on staggered couplings to steer correlations toward the ends of the chain. At the same time, Protocol 2 (P2) adopts a dual-port architecture that uses optimized boundary fields to mediate virtual excitations between terminal spins. Our results show that P2 consistently outperforms P1 in all spin values, generating higher-fidelity entanglement in shorter timescales when evaluated under the same system parameters. Furthermore, P2 exhibits superior robustness under realistic imperfections, including diagonal and off-diagonal disorder, as well as dephasing noise. To further assess the resilience of both protocols in experimentally relevant settings, we employ the pseudomode formalism to characterize the impact of non-Markovian noise on the entanglement dynamics. Our analysis reveals that the dual-port mechanism (P2) remains effective even when memory effects are present, as it reduces the excitation of bulk modes that would otherwise enhance environment-induced backflow. Together, the scalability, efficiency, and noise resilience of the dual-port approach position it as a promising framework for entanglement distribution in solid-state quantum information platforms. Full article
(This article belongs to the Special Issue Entanglement in Quantum Spin Systems)
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16 pages, 8218 KiB  
Article
Lead Induces Mitochondrial Dysregulation in SH-SY5Y Neuroblastoma Cells via a lncRNA/circRNA–miRNA–mRNA Interdependent Networks
by Yu Wang, Xuefeng Shen, Ruili Guan, Zaihua Zhao, Tao Wang, Yang Zhou, Xiaoming Chen, Jianbin Zhang, Wenjing Luo and Kejun Du
Int. J. Mol. Sci. 2025, 26(14), 6851; https://doi.org/10.3390/ijms26146851 - 17 Jul 2025
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Abstract
Lead (Pb) exposure poses a significant public health concern due to its neurotoxic effects. While mitochondrial dysfunction is implicated in lead neurotoxicity, the precise molecular mechanisms, particularly the role of non-coding RNA-mediated competing endogenous RNA networks, remain underexplored. SH-SY5Y neuroblastoma cells were treated [...] Read more.
Lead (Pb) exposure poses a significant public health concern due to its neurotoxic effects. While mitochondrial dysfunction is implicated in lead neurotoxicity, the precise molecular mechanisms, particularly the role of non-coding RNA-mediated competing endogenous RNA networks, remain underexplored. SH-SY5Y neuroblastoma cells were treated with 10 μM lead acetate. Cell viability was assessed by Cell Counting Kit-8 (CCK-8). Mitochondrial ultrastructure and quantity were analyzed via transmission electron microscopy (TEM). Key mitochondrial dynamics proteins were examined by Western blot. Comprehensive transcriptome sequencing, including long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), microRNAs (miRNAs) and mRNAs, was performed followed by functional enrichment and ceRNA network construction. Selected RNAs and hub genes were validated using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Lead exposure significantly reduced SH-SY5Y cell viability and induced mitochondrial damage (decreased quantity, swelling, fragmentation). Western blot confirmed an imbalance in mitochondrial dynamics, as indicated by decreased mitofusin 2 (MFN2), increased total and phosphorylated dynamin-related protein 1 (DRP1). Transcriptomic analysis revealed widespread differential expression of lncRNAs, circRNAs, miRNAs, and mRNAs. Enrichment analysis highlighted mitochondrial function and oxidative stress pathways. A ceRNA network identified five key hub genes: SLC7A11, FOS, HMOX1, HGF, and NR4A1. All validated RNA and hub gene expression patterns were consistent with sequencing results. Our study demonstrates that lead exposure significantly impairs mitochondrial quantity and morphology in SH-SY5Y cells, likely via disrupted mitochondrial dynamics. We reveal the potential regulatory mechanisms of lead-induced neurotoxicity involving ceRNA networks, identifying hub genes crucial for cellular stress response. This research provides a foundational framework for developing therapeutic strategies against lead-induced neurotoxicity. Full article
(This article belongs to the Section Molecular Genetics and Genomics)
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