Previous
Aim:
This study aimed to evaluate and compare the antioxidant activity, phenolic and flavonoid content, proline, and protein levels of oak honeydew and oak honeydew-nectar honeys produced in Northwestern Greece, providing the first comparative compositional data for these honey types.
Methods:
Thirty-four honey samples (16 oak honeydew and 18 oak honeydew-nectar) were collected from the region of Western Macedonia during the 2021–2022 harvest seasons. Total phenolic content (TPC), total flavonoid content (TFC), antioxidant activity (DPPH and FRAP assays), colour intensity (ABS450), and proline and protein contents were determined using spectrophotometric methods. Statistical analyses included independent-samples t-tests, Pearson correlation analysis, and multivariate techniques (PCA and hierarchical clustering) to assess variation and grouping patterns between honey types.
Results:
Oak honeydew honey showed higher TPC (137.52 vs. 115.69 mg GAE/100 g), antioxidant activity (DPPH: 20.26 vs. 15.24% inhibition; FRAP: 53.25 vs. 41.26 μΜ TE/100 g), and colour intensity (ABS450: 802 vs. 623.3 mAU) compared with oak honeydew-nectar honey (P < 0.05). TFC (51.67 vs. 42.22 mg RUE/100 g), proline (965.62 vs. 1,095.68 mg/kg), and protein contents (0.24 vs. 0.27 mg/g) were similar between oak honeydew and oak honeydew-nectar honey, respectively, with no significant differences (P > 0.05). Correlation analysis revealed strong positive associations among antioxidant activity, colour intensity, and flavonoid content, while protein exhibited inverse correlations with antioxidant parameters in oak honeydew honey but positive ones in oak honeydew-nectar honey. PCA showed a clear differentiation trend between the two honey types.
Conclusions:
Oak honeydew honey exhibited superior antioxidant capacity and phenolic content, reflecting a richer bioactive composition. These findings provide the first comparative insight into Greek oak honeys and highlight their practical significance for honey authentication, quality evaluation, and consumer awareness of honeydew honeys produced in Northwestern Greece.
Aim:
This study aimed to evaluate and compare the antioxidant activity, phenolic and flavonoid content, proline, and protein levels of oak honeydew and oak honeydew-nectar honeys produced in Northwestern Greece, providing the first comparative compositional data for these honey types.
Methods:
Thirty-four honey samples (16 oak honeydew and 18 oak honeydew-nectar) were collected from the region of Western Macedonia during the 2021–2022 harvest seasons. Total phenolic content (TPC), total flavonoid content (TFC), antioxidant activity (DPPH and FRAP assays), colour intensity (ABS450), and proline and protein contents were determined using spectrophotometric methods. Statistical analyses included independent-samples t-tests, Pearson correlation analysis, and multivariate techniques (PCA and hierarchical clustering) to assess variation and grouping patterns between honey types.
Results:
Oak honeydew honey showed higher TPC (137.52 vs. 115.69 mg GAE/100 g), antioxidant activity (DPPH: 20.26 vs. 15.24% inhibition; FRAP: 53.25 vs. 41.26 μΜ TE/100 g), and colour intensity (ABS450: 802 vs. 623.3 mAU) compared with oak honeydew-nectar honey (P < 0.05). TFC (51.67 vs. 42.22 mg RUE/100 g), proline (965.62 vs. 1,095.68 mg/kg), and protein contents (0.24 vs. 0.27 mg/g) were similar between oak honeydew and oak honeydew-nectar honey, respectively, with no significant differences (P > 0.05). Correlation analysis revealed strong positive associations among antioxidant activity, colour intensity, and flavonoid content, while protein exhibited inverse correlations with antioxidant parameters in oak honeydew honey but positive ones in oak honeydew-nectar honey. PCA showed a clear differentiation trend between the two honey types.
Conclusions:
Oak honeydew honey exhibited superior antioxidant capacity and phenolic content, reflecting a richer bioactive composition. These findings provide the first comparative insight into Greek oak honeys and highlight their practical significance for honey authentication, quality evaluation, and consumer awareness of honeydew honeys produced in Northwestern Greece.
DOI: https://doi.org/10.37349/eff.2026.1010108
The editor-in-chief plays a vital role in ensuring a journal’s scientific integrity and quality. Their primary responsibilities include managing the peer-review process, selecting qualified reviewers, and making final decisions on manuscript acceptance, revision, or rejection. In cases of scientific misconduct, conflicts of interest, authorship disputes, or ethical concerns, the editor has the ultimate authority.
An editor’s vision for the journal shapes which manuscripts are reviewed and accepted, influencing the journal’s academic direction. While the role offers benefits such as scientific prestige, greater research visibility, and financial compensation, it also entails significant ethical responsibilities. Academic editor malpractice refers to any actions that violate ethical standards or compromises the integrity of the peer-review process.
Editors typically serve five-year terms, often with the possibility of renewal, and are frequently evaluated based on the journal’s impact factor trend. However, their role extends beyond editorial duties—they act as gatekeepers, literary agents, accountants, mediators, and judges, navigating the complex relationships among authors, reviewers, and publishers.
Editors of major journals hold an extraordinary amount of power within the publication process. They act as an umpire to judge the scientific research that is being published. Like an umpire, they must know about the sport and rules of play, but they themselves should never be in the competition. The problem is that this ideal is not always met. Whether the subject is the efficacy of an antihypertensive drug, the value of a new costly biomarker, or the origin of a pandemic, editors often make decisions for multi-parametric—and also extra-scientific—reasons. On this basis, some papers are published while others are declined, and the stream of scientific evidence can be polluted.
In summary, the editor-in-chief is a cornerstone of academic publishing, ensuring that scientific quality and integrity are upheld while balancing multiple responsibilities.
The editor-in-chief plays a vital role in ensuring a journal’s scientific integrity and quality. Their primary responsibilities include managing the peer-review process, selecting qualified reviewers, and making final decisions on manuscript acceptance, revision, or rejection. In cases of scientific misconduct, conflicts of interest, authorship disputes, or ethical concerns, the editor has the ultimate authority.
An editor’s vision for the journal shapes which manuscripts are reviewed and accepted, influencing the journal’s academic direction. While the role offers benefits such as scientific prestige, greater research visibility, and financial compensation, it also entails significant ethical responsibilities. Academic editor malpractice refers to any actions that violate ethical standards or compromises the integrity of the peer-review process.
Editors typically serve five-year terms, often with the possibility of renewal, and are frequently evaluated based on the journal’s impact factor trend. However, their role extends beyond editorial duties—they act as gatekeepers, literary agents, accountants, mediators, and judges, navigating the complex relationships among authors, reviewers, and publishers.
Editors of major journals hold an extraordinary amount of power within the publication process. They act as an umpire to judge the scientific research that is being published. Like an umpire, they must know about the sport and rules of play, but they themselves should never be in the competition. The problem is that this ideal is not always met. Whether the subject is the efficacy of an antihypertensive drug, the value of a new costly biomarker, or the origin of a pandemic, editors often make decisions for multi-parametric—and also extra-scientific—reasons. On this basis, some papers are published while others are declined, and the stream of scientific evidence can be polluted.
In summary, the editor-in-chief is a cornerstone of academic publishing, ensuring that scientific quality and integrity are upheld while balancing multiple responsibilities.
DOI: https://doi.org/10.37349/ec.2026.101286
Exercise-related arrhythmia is attracting growing attention, according to the increased popularity of leisure-time sports, which have great benefits and acute risk, although the hemodynamics and therapeutics of exercise-related arrhythmia are poorly understood. We have experienced two cases of different types of exercise-related arrhythmias. In an 80-year-old woman, exercise-induced increase in supraventricular premature contractions (SVPCs) converted to atrial fibrillation (AF) during a control ergometric stress test (EST), but SVPCs were diminished, and AF was not observed in the secondary EST after starting bisoprolol. In a 39-year-old woman, idiopathic premature ventricular contractions (PVCs) appeared immediately after the termination of the control EST but were scarcely induced by the secondary EST under the treatment with bisoprolol. Post-exercise abnormal increase in the double product was suppressed, leading to the possibility of improved exercise tolerance in both cases. A couple of ESTs under the same protocol to compare the arrhythmic behaviors with and without treatment provides a therapeutic strategy in exercise-related arrhythmia, and short-term bisoprolol is concluded to be favorable to the specific types of exercise-related arrhythmia, at least in these two cases.
Exercise-related arrhythmia is attracting growing attention, according to the increased popularity of leisure-time sports, which have great benefits and acute risk, although the hemodynamics and therapeutics of exercise-related arrhythmia are poorly understood. We have experienced two cases of different types of exercise-related arrhythmias. In an 80-year-old woman, exercise-induced increase in supraventricular premature contractions (SVPCs) converted to atrial fibrillation (AF) during a control ergometric stress test (EST), but SVPCs were diminished, and AF was not observed in the secondary EST after starting bisoprolol. In a 39-year-old woman, idiopathic premature ventricular contractions (PVCs) appeared immediately after the termination of the control EST but were scarcely induced by the secondary EST under the treatment with bisoprolol. Post-exercise abnormal increase in the double product was suppressed, leading to the possibility of improved exercise tolerance in both cases. A couple of ESTs under the same protocol to compare the arrhythmic behaviors with and without treatment provides a therapeutic strategy in exercise-related arrhythmia, and short-term bisoprolol is concluded to be favorable to the specific types of exercise-related arrhythmia, at least in these two cases.
DOI: https://doi.org/10.37349/ec.2026.101287
This article belongs to the special issue Exploring Exercise Cardiology: from Molecules to Humans
Digital twin technology is emerging as a transformative paradigm in healthcare, shifting practice from provider-centered models toward more personalized forms of medicine. As dynamic virtual representations of the human body, digital twins integrate biometric data, lifestyle patterns, and clinical records to simulate, monitor, and predict health trajectories in real time. Their growing use raises not only technical possibilities but also important questions about how patients relate to these data-driven counterparts, particularly when twins inform everyday health decisions in chronic care, such as diabetes or oncology. This perspective examines these relational dynamics and their ethical, cultural, and experiential implications for autonomy, decision-making, and the lived experience of being represented in data. To guide this analysis, we introduce a scale framework with three intersecting lenses: time, distinguishing asynchronous from synchronous updating; twining, ranging from close mirroring to more augmentative forms of representation; and control, spanning human-led to twin-driven decision authority. Using this framework, we position four common types of digital twins: mirror, shadow, intelligent, and simulacra as an evolution from basic representation to transformative modeling. We argue that future healthcare and public health policy must go beyond technical innovation to address patients’ lived experiences, ensuring that digital twins enhance rather than diminish autonomy, trust, and equity. This perspective thus calls for a patient-centered approach in designing and implementing digital twin technologies.
Digital twin technology is emerging as a transformative paradigm in healthcare, shifting practice from provider-centered models toward more personalized forms of medicine. As dynamic virtual representations of the human body, digital twins integrate biometric data, lifestyle patterns, and clinical records to simulate, monitor, and predict health trajectories in real time. Their growing use raises not only technical possibilities but also important questions about how patients relate to these data-driven counterparts, particularly when twins inform everyday health decisions in chronic care, such as diabetes or oncology. This perspective examines these relational dynamics and their ethical, cultural, and experiential implications for autonomy, decision-making, and the lived experience of being represented in data. To guide this analysis, we introduce a scale framework with three intersecting lenses: time, distinguishing asynchronous from synchronous updating; twining, ranging from close mirroring to more augmentative forms of representation; and control, spanning human-led to twin-driven decision authority. Using this framework, we position four common types of digital twins: mirror, shadow, intelligent, and simulacra as an evolution from basic representation to transformative modeling. We argue that future healthcare and public health policy must go beyond technical innovation to address patients’ lived experiences, ensuring that digital twins enhance rather than diminish autonomy, trust, and equity. This perspective thus calls for a patient-centered approach in designing and implementing digital twin technologies.
DOI: https://doi.org/10.37349/edht.2026.101181
Background:
Vascular aging is a major driver of cardiovascular, metabolic, and degenerative diseases, characterized by oxidative stress, mitochondrial dysfunction, endothelial senescence, and impaired proteostasis. Emerging data show that anti-infective drugs can influence these aging pathways beyond antimicrobial activity. However, their capacity to accelerate or slow vascular ageing has not been clearly defined. This review summarizes current evidence on how anti-infective agents modulate vascular ageing mechanisms.
Methods:
A systematic review was conducted following PRISMA 2020 guidelines. Studies from 2000 to 2024 were searched in major indexed databases. Eligible studies included in vitro, animal, and human research evaluating the effects of anti-infective agents on endothelial function, vascular senescence markers (p16INK4a, p21, SA-β-gal), oxidative stress, mitochondrial activity, inflammation, or proteostasis, key determinants of vascular ageing. Studies lacking mechanistic aging endpoints were excluded. Extracted data included drug class, model type, study design, and age-related outcomes. Risk of bias was assessed using SYRCLE, RoB-2, ROBINS-I, and narrative appraisal for in vitro studies.
Results:
Ninety-eight studies were identified; after removing six duplicates, ninety-two met the criteria. Macrolides, tetracyclines, and selected antivirals exerted anti-ageing effects by suppressing senescence-associated secretory phenotype (SASP), preserving mitochondrial integrity, reducing oxidative stress, and enhancing autophagy. Aminoglycosides and fluoroquinolones accelerated vascular ageing by generating reactive oxygen species, inducing DNA damage, and disrupting proteostasis. Antiviral protease inhibitors worsened endothelial dysfunction and metabolic aging. Antifungals such as itraconazole and amphotericin B impaired mitochondrial activity and angiogenesis, contributing to ageing phenotypes. Antiparasitic drugs showed mixed aging outcomes: chloroquine promoted autophagy and longevity, whereas thiabendazole impaired vascular stability. Broad-spectrum antibiotics disrupted the gut-vascular axis, increasing trimethylamine N-oxide, a mediator of inflammatory vascular aging.
Discussion:
Anti-infective drugs display diverse, class-specific effects on vascular aging. Recognizing these age-related actions is essential for safer prescribing and for repurposing anti-infective agents to target pathological vascular aging mechanisms.
Background:
Vascular aging is a major driver of cardiovascular, metabolic, and degenerative diseases, characterized by oxidative stress, mitochondrial dysfunction, endothelial senescence, and impaired proteostasis. Emerging data show that anti-infective drugs can influence these aging pathways beyond antimicrobial activity. However, their capacity to accelerate or slow vascular ageing has not been clearly defined. This review summarizes current evidence on how anti-infective agents modulate vascular ageing mechanisms.
Methods:
A systematic review was conducted following PRISMA 2020 guidelines. Studies from 2000 to 2024 were searched in major indexed databases. Eligible studies included in vitro, animal, and human research evaluating the effects of anti-infective agents on endothelial function, vascular senescence markers (p16INK4a, p21, SA-β-gal), oxidative stress, mitochondrial activity, inflammation, or proteostasis, key determinants of vascular ageing. Studies lacking mechanistic aging endpoints were excluded. Extracted data included drug class, model type, study design, and age-related outcomes. Risk of bias was assessed using SYRCLE, RoB-2, ROBINS-I, and narrative appraisal for in vitro studies.
Results:
Ninety-eight studies were identified; after removing six duplicates, ninety-two met the criteria. Macrolides, tetracyclines, and selected antivirals exerted anti-ageing effects by suppressing senescence-associated secretory phenotype (SASP), preserving mitochondrial integrity, reducing oxidative stress, and enhancing autophagy. Aminoglycosides and fluoroquinolones accelerated vascular ageing by generating reactive oxygen species, inducing DNA damage, and disrupting proteostasis. Antiviral protease inhibitors worsened endothelial dysfunction and metabolic aging. Antifungals such as itraconazole and amphotericin B impaired mitochondrial activity and angiogenesis, contributing to ageing phenotypes. Antiparasitic drugs showed mixed aging outcomes: chloroquine promoted autophagy and longevity, whereas thiabendazole impaired vascular stability. Broad-spectrum antibiotics disrupted the gut-vascular axis, increasing trimethylamine N-oxide, a mediator of inflammatory vascular aging.
Discussion:
Anti-infective drugs display diverse, class-specific effects on vascular aging. Recognizing these age-related actions is essential for safer prescribing and for repurposing anti-infective agents to target pathological vascular aging mechanisms.
DOI: https://doi.org/10.37349/eds.2026.1008143
Aim:
Polypharmacy is a major health concern among older adults and is associated with increased vulnerability and adverse health outcomes. However, limited evidence exists regarding its association with sensory, oral, and dietary functions. This study examined the effects of polypharmacy on these functions using nationally representative data from the 2023 Korean Elderly Survey.
Methods:
A total of 10,078 community-dwelling adults aged ≥ 65 years were analyzed. Polypharmacy was defined as the use of five or more medications. Sensory function (vision and hearing), oral function (chewing difficulty, swallowing difficulty, denture use, unmet dental needs), and dietary intake (meal frequency, fruit and vegetable consumption) were assessed using structured questionnaires. Chi-square tests and logistic regression analyses were performed. Model 1 adjusted for demographic factors, and Model 2 additionally adjusted for the number of chronic diseases.
Results:
Older adults with polypharmacy showed substantially poorer sensory and oral function than those without polypharmacy. Higher prevalence was observed for vision difficulty (60.5% vs. 40.6%), hearing difficulty (48.7% vs. 20.6%), chewing difficulty (58.9% vs. 30.1%), swallowing difficulty (20.9% vs. 6.7%), and unmet dental care needs (9.6% vs. 3.0%) (all p < 0.001). In the fully adjusted model, polypharmacy remained significantly associated with hearing difficulty, chewing difficulty, swallowing difficulty, denture use, and unmet dental care needs. However, associations between polypharmacy and dietary intake indicators were not statistically significant after adjustment.
Conclusions:
Polypharmacy is significantly associated with hearing and oral functional impairments among older adults, and these associations were attenuated but not fully explained after adjusting for chronic disease burden. These findings highlight the importance of comprehensive geriatric assessment and multidisciplinary care that integrates medication management and oral health. Strategies promoting rational prescribing and monitoring of functional outcomes are essential to mitigate the adverse effects of polypharmacy and support healthy aging.
Aim:
Polypharmacy is a major health concern among older adults and is associated with increased vulnerability and adverse health outcomes. However, limited evidence exists regarding its association with sensory, oral, and dietary functions. This study examined the effects of polypharmacy on these functions using nationally representative data from the 2023 Korean Elderly Survey.
Methods:
A total of 10,078 community-dwelling adults aged ≥ 65 years were analyzed. Polypharmacy was defined as the use of five or more medications. Sensory function (vision and hearing), oral function (chewing difficulty, swallowing difficulty, denture use, unmet dental needs), and dietary intake (meal frequency, fruit and vegetable consumption) were assessed using structured questionnaires. Chi-square tests and logistic regression analyses were performed. Model 1 adjusted for demographic factors, and Model 2 additionally adjusted for the number of chronic diseases.
Results:
Older adults with polypharmacy showed substantially poorer sensory and oral function than those without polypharmacy. Higher prevalence was observed for vision difficulty (60.5% vs. 40.6%), hearing difficulty (48.7% vs. 20.6%), chewing difficulty (58.9% vs. 30.1%), swallowing difficulty (20.9% vs. 6.7%), and unmet dental care needs (9.6% vs. 3.0%) (all p < 0.001). In the fully adjusted model, polypharmacy remained significantly associated with hearing difficulty, chewing difficulty, swallowing difficulty, denture use, and unmet dental care needs. However, associations between polypharmacy and dietary intake indicators were not statistically significant after adjustment.
Conclusions:
Polypharmacy is significantly associated with hearing and oral functional impairments among older adults, and these associations were attenuated but not fully explained after adjusting for chronic disease burden. These findings highlight the importance of comprehensive geriatric assessment and multidisciplinary care that integrates medication management and oral health. Strategies promoting rational prescribing and monitoring of functional outcomes are essential to mitigate the adverse effects of polypharmacy and support healthy aging.
DOI: https://doi.org/10.37349/emed.2026.1001380
Aim:
Diagnosing and treating major depressive disorder (MDD) remains a pressing global health challenge. Generative-AI tools, by lowering technical barriers and offering rapid visual feedback, may open new avenues for art-based assessment and intervention.
Methods:
In this exploratory qualitative pilot, we conducted reflexive thematic analysis of semi-structured interviews with N = 10 young adults at elevated risk for depression who generated self-representative images in Midjourney during a 45-minute session. Participants were selected from a larger cohort described elsewhere; no quantitative analyses were conducted in the present paper.
Results:
Qualitative findings suggested therapeutic-like mechanisms that mirror—and in some cases amplify—those reported for traditional art therapy, including the experience of flow and spontaneity, a heightened sense of creative agency, and the safe externalization of difficult or extreme emotions. Some participants described abrupt “sentiment switches,” where joyful imagery was immediately followed by scenes of sudden, intrusive self-criticism. Importantly, the generative process also surfaced idiosyncratic “resource images” (e.g., nature motifs, hobbies, values, loved ones) that participants experienced as calming or empowering, hinting at personalised anchors for future interventions.
Conclusions:
In line with prior quantitative work showing that more negative prompt sentiment statistically relates to higher BDI scores, the present qualitative narratives offer an interpretive account of how such negativity may emerge during AI-assisted self-representation. However, the current study does not integrate datasets or perform mixed-methods triangulation and uses those prior findings solely for contextualization. We conclude that, with appropriate ethical safeguards, generative-AI image making may serve as a flexible, low-cost adjunct to existing diagnostic and art-therapeutic practices, offering clients and clinicians a shared visual language for exploring the multi-layered experience of depression.
Aim:
Diagnosing and treating major depressive disorder (MDD) remains a pressing global health challenge. Generative-AI tools, by lowering technical barriers and offering rapid visual feedback, may open new avenues for art-based assessment and intervention.
Methods:
In this exploratory qualitative pilot, we conducted reflexive thematic analysis of semi-structured interviews with N = 10 young adults at elevated risk for depression who generated self-representative images in Midjourney during a 45-minute session. Participants were selected from a larger cohort described elsewhere; no quantitative analyses were conducted in the present paper.
Results:
Qualitative findings suggested therapeutic-like mechanisms that mirror—and in some cases amplify—those reported for traditional art therapy, including the experience of flow and spontaneity, a heightened sense of creative agency, and the safe externalization of difficult or extreme emotions. Some participants described abrupt “sentiment switches,” where joyful imagery was immediately followed by scenes of sudden, intrusive self-criticism. Importantly, the generative process also surfaced idiosyncratic “resource images” (e.g., nature motifs, hobbies, values, loved ones) that participants experienced as calming or empowering, hinting at personalised anchors for future interventions.
Conclusions:
In line with prior quantitative work showing that more negative prompt sentiment statistically relates to higher BDI scores, the present qualitative narratives offer an interpretive account of how such negativity may emerge during AI-assisted self-representation. However, the current study does not integrate datasets or perform mixed-methods triangulation and uses those prior findings solely for contextualization. We conclude that, with appropriate ethical safeguards, generative-AI image making may serve as a flexible, low-cost adjunct to existing diagnostic and art-therapeutic practices, offering clients and clinicians a shared visual language for exploring the multi-layered experience of depression.
DOI: https://doi.org/10.37349/edht.2026.101180
This article belongs to the special issue Digital Health Innovations in the Battle Against Psychological Problems: Progress, Hurdles, and Prospects
Pulsed radiofrequency (PRF) has emerged as a promising and versatile technology in pain management and immunological modulation. PRFʼs effects extend beyond pain modulation, demonstrating the ability to regulate inflammatory processes through cytokine modulation, reduction of microglial hyperactivity, and promotion of autophagy. These mechanisms position PRF as a potential therapeutic tool not only for neuropathic and musculoskeletal pain but also for conditions associated with neuroinflammation and immune dysfunction, including chronic inflammatory and degenerative diseases. Clinically, PRF has demonstrated potential in alleviating neuropathic pain in several clinical studies—including a limited number of small RCTs. However, most of the available evidence remains of low methodological quality, with many studies being observational, retrospective, or underpowered. Moreover, the lack of standardized protocols remains a barrier to its broader adoption. Establishing evidence-based guidelines and enhancing practitioner expertise are critical to ensuring consistent and optimal patient outcomes. Future research should focus on optimizing PRF technical parameters, elucidating molecular mechanisms, and expanding its clinical applications. Integrating PRF with emerging therapies, such as orthobiologics, biological drugs, and electrical stimulation, may further enhance its efficacy. Moreover, advancements in predictive biomarkers and device technologies hold promise for personalized treatments, improving the precision and effectiveness of PRF interventions. This narrative review explores the primary clinical applications, underlying biological mechanisms, and potential future directions of PRF, emphasizing its ability to address complex therapeutic challenges.
Pulsed radiofrequency (PRF) has emerged as a promising and versatile technology in pain management and immunological modulation. PRFʼs effects extend beyond pain modulation, demonstrating the ability to regulate inflammatory processes through cytokine modulation, reduction of microglial hyperactivity, and promotion of autophagy. These mechanisms position PRF as a potential therapeutic tool not only for neuropathic and musculoskeletal pain but also for conditions associated with neuroinflammation and immune dysfunction, including chronic inflammatory and degenerative diseases. Clinically, PRF has demonstrated potential in alleviating neuropathic pain in several clinical studies—including a limited number of small RCTs. However, most of the available evidence remains of low methodological quality, with many studies being observational, retrospective, or underpowered. Moreover, the lack of standardized protocols remains a barrier to its broader adoption. Establishing evidence-based guidelines and enhancing practitioner expertise are critical to ensuring consistent and optimal patient outcomes. Future research should focus on optimizing PRF technical parameters, elucidating molecular mechanisms, and expanding its clinical applications. Integrating PRF with emerging therapies, such as orthobiologics, biological drugs, and electrical stimulation, may further enhance its efficacy. Moreover, advancements in predictive biomarkers and device technologies hold promise for personalized treatments, improving the precision and effectiveness of PRF interventions. This narrative review explores the primary clinical applications, underlying biological mechanisms, and potential future directions of PRF, emphasizing its ability to address complex therapeutic challenges.
DOI: https://doi.org/10.37349/ei.2026.1003235
Osteoporosis is a disabling disease with a significant impact on the global population, particularly among older men and postmenopausal women. Several factors contribute to the increasing prevalence of osteoporosis, including greater life expectancy and the absence of symptoms in its early stages. The morbidity, mortality, and substantial economic burden associated with osteoporosis, especially due to hip fractures and related complications, constitute a major public health concern. Diagnosis should involve a comprehensive biochemical profile, along with additional tests to rule out secondary causes, which are often underdiagnosed and can influence the progression of the disease. Preventive measures and early diagnosis are essential to maintaining bone health and preventing fractures and disability. This review will focus on the definition, diagnostic approach, and key considerations prior to initiating treatment in patients with osteoporosis. Fracture risk prediction tools, including Fracture Risk Assessment Tool (FRAX), and treatment strategies are not addressed, as this review focuses on the appropriate diagnostic evaluation of osteoporosis and the systematic exclusion of secondary causes.
Osteoporosis is a disabling disease with a significant impact on the global population, particularly among older men and postmenopausal women. Several factors contribute to the increasing prevalence of osteoporosis, including greater life expectancy and the absence of symptoms in its early stages. The morbidity, mortality, and substantial economic burden associated with osteoporosis, especially due to hip fractures and related complications, constitute a major public health concern. Diagnosis should involve a comprehensive biochemical profile, along with additional tests to rule out secondary causes, which are often underdiagnosed and can influence the progression of the disease. Preventive measures and early diagnosis are essential to maintaining bone health and preventing fractures and disability. This review will focus on the definition, diagnostic approach, and key considerations prior to initiating treatment in patients with osteoporosis. Fracture risk prediction tools, including Fracture Risk Assessment Tool (FRAX), and treatment strategies are not addressed, as this review focuses on the appropriate diagnostic evaluation of osteoporosis and the systematic exclusion of secondary causes.
DOI: https://doi.org/10.37349/eemd.2026.101456
Background:
Metabolic syndrome and dyslipidaemia increase the risk of death by two or three times. In this context, the role of apolipoprotein A-I (Apo A-I), the main structural protein of high-density lipoprotein (HDL), stands out, since its anti-inflammatory potential reduces cardiovascular risk. Further, genetic modifications, such as the rs670 single-nucleotide polymorphism (SNP), in the promoter region of the APOA1 gene are associated with the development of cardiovascular events, dyslipidemia, and diabetes, as well as metabolic syndrome. Thus, this study aims to investigate the relation between the occurrence of dyslipidemia and the rs670 SNP genotypes.
Methods:
An integrative and systematic review was performed with the LitVar2 database according to the PRISMA protocol standards. Studies were researched up to August 2025. Then, a meta-analysis was performed using the fixed-effects model, since the study was considered homogeneous based on the I2 value (< 50%).
Results:
Of the 99 found articles in the database, 5 referred to metabolic disorders (n = 7,705—4 Chinese studies and 1 Iranian study) and were published between 2015 and 2018. Three (n = 2,784 patients or 36.13%) of the articles indicated an association between the polymorphic allele and a higher risk of developing dyslipidemia with a relative risk of 1.16 (IC 95% 1.09–1.23, p < 0.01, I2 = 0%). Relative risk (IC 95%) was presented, and p < 0.05 was defined as the significance criterion.
Discussion:
This study reinforces a possible association between the influence of SNP rs670 and dyslipidemia. This emphasizes the importance of conducting further research incorporating a larger and more diverse study group, as well as investigating the genetic and environmental influence on the phenotypic expression of the rs670 SNP.
Background:
Metabolic syndrome and dyslipidaemia increase the risk of death by two or three times. In this context, the role of apolipoprotein A-I (Apo A-I), the main structural protein of high-density lipoprotein (HDL), stands out, since its anti-inflammatory potential reduces cardiovascular risk. Further, genetic modifications, such as the rs670 single-nucleotide polymorphism (SNP), in the promoter region of the APOA1 gene are associated with the development of cardiovascular events, dyslipidemia, and diabetes, as well as metabolic syndrome. Thus, this study aims to investigate the relation between the occurrence of dyslipidemia and the rs670 SNP genotypes.
Methods:
An integrative and systematic review was performed with the LitVar2 database according to the PRISMA protocol standards. Studies were researched up to August 2025. Then, a meta-analysis was performed using the fixed-effects model, since the study was considered homogeneous based on the I2 value (< 50%).
Results:
Of the 99 found articles in the database, 5 referred to metabolic disorders (n = 7,705—4 Chinese studies and 1 Iranian study) and were published between 2015 and 2018. Three (n = 2,784 patients or 36.13%) of the articles indicated an association between the polymorphic allele and a higher risk of developing dyslipidemia with a relative risk of 1.16 (IC 95% 1.09–1.23, p < 0.01, I2 = 0%). Relative risk (IC 95%) was presented, and p < 0.05 was defined as the significance criterion.
Discussion:
This study reinforces a possible association between the influence of SNP rs670 and dyslipidemia. This emphasizes the importance of conducting further research incorporating a larger and more diverse study group, as well as investigating the genetic and environmental influence on the phenotypic expression of the rs670 SNP.
DOI: https://doi.org/10.37349/eemd.2026.101455
Aim:
The prevalence of multidrug-resistant “superbugs”, particularly Acinetobacter baumannii and Klebsiella pneumoniae, is a menacing phenomenon in society, rendering last-resort antibiotics increasingly suboptimal and ineffective. Carbapenemase enzymes play a major role in this resistance by hydrolysing carbapenem antibiotics. This study aims to identify and characterize potential non-covalent carbapenemase inhibitors using multiscale computational approaches.
Methods:
A focused library of 245 compounds, comprising pharmacopeial derivatives and chemogenomic molecules, was screened using a hierarchical virtual screening workflow. Top-ranked hits were further evaluated by rescoring for thermodynamic affinity. The most promising candidate was subjected to a 100 ns molecular dynamics (MD) simulation to assess binding stability, followed by Well-Tempered Metadynamics (WTMetaD) to characterise the free energy landscape and binding behaviour. Pharmacokinetic and toxicity profiles were predicted using SwissADME and ProTox 3.0.
Results:
Three compounds, daunorubicin, doxorubicin, and EUB0000226b, emerged as potential carbapenemase inhibitors. EUB0000226b demonstrated the most favourable binding affinity and structural novelty. MD simulations showed protein stability, while ligand RMSD fluctuations (2.4–5.6 Å) suggested flexible binding. WTMetaD analysis revealed a solvent-separated metastable state that increased ligand residence time within the active site. ADME and toxicity predictions indicated acceptable drug-likeness, good gastrointestinal absorption, and a generally safe profile.
Conclusions:
Multiscale computational analysis identified EUB0000226b as a promising non-covalent carbapenemase inhibitor with favourable binding energetics, dynamic stability, and drug-like properties. These findings support its further experimental validation and potential development for combating carbapenem-resistant bacterial pathogens.
Aim:
The prevalence of multidrug-resistant “superbugs”, particularly Acinetobacter baumannii and Klebsiella pneumoniae, is a menacing phenomenon in society, rendering last-resort antibiotics increasingly suboptimal and ineffective. Carbapenemase enzymes play a major role in this resistance by hydrolysing carbapenem antibiotics. This study aims to identify and characterize potential non-covalent carbapenemase inhibitors using multiscale computational approaches.
Methods:
A focused library of 245 compounds, comprising pharmacopeial derivatives and chemogenomic molecules, was screened using a hierarchical virtual screening workflow. Top-ranked hits were further evaluated by rescoring for thermodynamic affinity. The most promising candidate was subjected to a 100 ns molecular dynamics (MD) simulation to assess binding stability, followed by Well-Tempered Metadynamics (WTMetaD) to characterise the free energy landscape and binding behaviour. Pharmacokinetic and toxicity profiles were predicted using SwissADME and ProTox 3.0.
Results:
Three compounds, daunorubicin, doxorubicin, and EUB0000226b, emerged as potential carbapenemase inhibitors. EUB0000226b demonstrated the most favourable binding affinity and structural novelty. MD simulations showed protein stability, while ligand RMSD fluctuations (2.4–5.6 Å) suggested flexible binding. WTMetaD analysis revealed a solvent-separated metastable state that increased ligand residence time within the active site. ADME and toxicity predictions indicated acceptable drug-likeness, good gastrointestinal absorption, and a generally safe profile.
Conclusions:
Multiscale computational analysis identified EUB0000226b as a promising non-covalent carbapenemase inhibitor with favourable binding energetics, dynamic stability, and drug-like properties. These findings support its further experimental validation and potential development for combating carbapenem-resistant bacterial pathogens.
DOI: https://doi.org/10.37349/eds.2026.1008140
This article belongs to the special issue Discovery and development of new antibacterial compounds
Immunotherapy has transformed oncology, yet has only been marginally effective in prostate cancer (PCa), which is a malignancy with a low mutational load and a highly immunosuppressive tumor microenvironment (TME). This critical review is a reflection on the changing position of the innovative immunotherapies in PCa that extends beyond the description stage to synthesize the synergies and constraints of immune checkpoint inhibitors (ICIs), chimeric antigen receptor (CAR) T-cell therapy, and next-generation modalities such as bispecific T-cell engagers (BiTEs). We assess the mechanistic reasoning of combination therapies, comprising androgen receptor signaling communicators, PARP communicators, and radioligand therapies, which seek to modulate the immunogenicity of the immune-cold PCa TME. Also, we combine new knowledge to novel resistance pathways, including the newly discovered thrombospondin-1-CD47 axis, in the process of T cell exhaustion through calcineurin-NFAT signaling. Although some preclinical data and initial clinical indicators in biomarker-selected subpopulations are promising, the vast majority of Phase III trials of ICIs in unselected populations with metastatic castration-resistant prostate cancer (mCRPC) have failed. This review reveals that the next generation of PCa immunotherapy would not be sequential monotherapies but rather rationally designed multimodal combinations guided by profound molecular and immune profiling to overcome inherent resistance mechanisms.
Immunotherapy has transformed oncology, yet has only been marginally effective in prostate cancer (PCa), which is a malignancy with a low mutational load and a highly immunosuppressive tumor microenvironment (TME). This critical review is a reflection on the changing position of the innovative immunotherapies in PCa that extends beyond the description stage to synthesize the synergies and constraints of immune checkpoint inhibitors (ICIs), chimeric antigen receptor (CAR) T-cell therapy, and next-generation modalities such as bispecific T-cell engagers (BiTEs). We assess the mechanistic reasoning of combination therapies, comprising androgen receptor signaling communicators, PARP communicators, and radioligand therapies, which seek to modulate the immunogenicity of the immune-cold PCa TME. Also, we combine new knowledge to novel resistance pathways, including the newly discovered thrombospondin-1-CD47 axis, in the process of T cell exhaustion through calcineurin-NFAT signaling. Although some preclinical data and initial clinical indicators in biomarker-selected subpopulations are promising, the vast majority of Phase III trials of ICIs in unselected populations with metastatic castration-resistant prostate cancer (mCRPC) have failed. This review reveals that the next generation of PCa immunotherapy would not be sequential monotherapies but rather rationally designed multimodal combinations guided by profound molecular and immune profiling to overcome inherent resistance mechanisms.
DOI: https://doi.org/10.37349/eds.2026.1008141
DOI: https://doi.org/10.37349/eds.2026.1008142
Endocrine hypertension (HT) includes a group of secondary hypertensive disorders caused by hormonal excess, primarily primary aldosteronism (PA), pheochromocytoma and paraganglioma (PPGL), and Cushing syndrome (CS). Although relatively uncommon, these conditions confer a disproportionately high cardiovascular risk that extends beyond blood pressure elevation. Aldosterone, catecholamines, and cortisol each induce myocardial fibrosis, oxidative stress, and endothelial dysfunction, leading to left ventricular hypertrophy (LVH), arrhythmias, and heart failure. In PA, chronic aldosterone excess activates mineralocorticoid receptors in cardiac and vascular tissues, promoting collagen deposition, diastolic dysfunction, and atrial fibrillation (AF) that may regress after adrenalectomy or pharmacologic blockade. PPGL causes episodic catecholamine surges resulting in β-adrenergic overstimulation, calcium overload, and microvascular ischemia, producing reversible or sometimes persistent catecholamine-induced cardiotoxicity. CS induces concentric hypertrophy, metabolic derangements, and vascular injury through prolonged glucocorticoid exposure, with cardiovascular recovery often incomplete after biochemical remission. Despite distinct hormonal origins, these disorders share convergent mechanisms, including fibroblast activation, mitochondrial injury, and maladaptive remodeling, that define endocrine cardiomyopathy. Early detection and targeted hormonal treatment can reverse much of the cardiac and vascular damage, whereas delayed recognition leads to irreversible fibrosis and persistent diastolic dysfunction. Recognition of these hormone-specific mechanisms is crucial for clinicians to anticipate, manage, and prevent these deleterious cardiovascular effects. Advances in molecular genetics, cardiac imaging, and biomarker research are improving our understanding of genotype-phenotype relationships and long-term reversibility of injury. Endocrine HT should therefore be recognized as a systemic cardiovascular disorder in which hormonal excess functions as a primary pathogenic driver; timely diagnosis and multidisciplinary care remain key to reducing morbidity and mortality.
Endocrine hypertension (HT) includes a group of secondary hypertensive disorders caused by hormonal excess, primarily primary aldosteronism (PA), pheochromocytoma and paraganglioma (PPGL), and Cushing syndrome (CS). Although relatively uncommon, these conditions confer a disproportionately high cardiovascular risk that extends beyond blood pressure elevation. Aldosterone, catecholamines, and cortisol each induce myocardial fibrosis, oxidative stress, and endothelial dysfunction, leading to left ventricular hypertrophy (LVH), arrhythmias, and heart failure. In PA, chronic aldosterone excess activates mineralocorticoid receptors in cardiac and vascular tissues, promoting collagen deposition, diastolic dysfunction, and atrial fibrillation (AF) that may regress after adrenalectomy or pharmacologic blockade. PPGL causes episodic catecholamine surges resulting in β-adrenergic overstimulation, calcium overload, and microvascular ischemia, producing reversible or sometimes persistent catecholamine-induced cardiotoxicity. CS induces concentric hypertrophy, metabolic derangements, and vascular injury through prolonged glucocorticoid exposure, with cardiovascular recovery often incomplete after biochemical remission. Despite distinct hormonal origins, these disorders share convergent mechanisms, including fibroblast activation, mitochondrial injury, and maladaptive remodeling, that define endocrine cardiomyopathy. Early detection and targeted hormonal treatment can reverse much of the cardiac and vascular damage, whereas delayed recognition leads to irreversible fibrosis and persistent diastolic dysfunction. Recognition of these hormone-specific mechanisms is crucial for clinicians to anticipate, manage, and prevent these deleterious cardiovascular effects. Advances in molecular genetics, cardiac imaging, and biomarker research are improving our understanding of genotype-phenotype relationships and long-term reversibility of injury. Endocrine HT should therefore be recognized as a systemic cardiovascular disorder in which hormonal excess functions as a primary pathogenic driver; timely diagnosis and multidisciplinary care remain key to reducing morbidity and mortality.
DOI: https://doi.org/10.37349/eemd.2026.101454
The symptoms of atopic dermatitis (AD), a chronic, recurrent inflammatory skin condition, include immunological dysregulation, severe pruritus, and malfunctioning of the epidermal barrier. Recent developments in our understanding of AD’s molecular and immunological pathways have shed light on the functions of cytokines, including interleukin (IL)-4, IL-13, IL-31, and IL-22, as well as the impact of genetic mutations in filaggrin and other barrier proteins. Inflammation and barrier dysfunction are further aggravated by microbial dysbiosis, especially colonisation of Staphylococcus aureus. Treatment options include topical corticosteroids, topical calcineurin inhibitors, targeted biologics, and small-molecule inhibitors that alter the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and phosphodiesterase 4 (PDE4) pathways, as well as Mn- and Fe-porphyrin ring-based topical formulations. Even with these advancements, tailored treatment and long-term illness control are still challenging to achieve. New strategies that emphasise gene therapy and microbiome restoration can potentially improve the accuracy and comprehensiveness of AD treatment.
The symptoms of atopic dermatitis (AD), a chronic, recurrent inflammatory skin condition, include immunological dysregulation, severe pruritus, and malfunctioning of the epidermal barrier. Recent developments in our understanding of AD’s molecular and immunological pathways have shed light on the functions of cytokines, including interleukin (IL)-4, IL-13, IL-31, and IL-22, as well as the impact of genetic mutations in filaggrin and other barrier proteins. Inflammation and barrier dysfunction are further aggravated by microbial dysbiosis, especially colonisation of Staphylococcus aureus. Treatment options include topical corticosteroids, topical calcineurin inhibitors, targeted biologics, and small-molecule inhibitors that alter the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and phosphodiesterase 4 (PDE4) pathways, as well as Mn- and Fe-porphyrin ring-based topical formulations. Even with these advancements, tailored treatment and long-term illness control are still challenging to achieve. New strategies that emphasise gene therapy and microbiome restoration can potentially improve the accuracy and comprehensiveness of AD treatment.
DOI: https://doi.org/10.37349/eaa.2026.1009105
This article belongs to the special issue Atopic Dermatitis – Pathology and Treatment Modalities
Aim:
A comprehensive understanding of current digital literacy and perspectives of the psychiatric workforce is important to introduce appropriate digital psychiatry interventions and implement contextually relevant measures in Pakistan. This study aims to address a gap in the existing literature by assessing psychiatrists’ knowledge, attitudes, perceived barriers, and willingness to integrate digital psychiatry into their clinical practice.
Methods:
A cross-sectional online survey was conducted from January 2023 to June 2023 across psychiatric departments of 18 public hospitals in Pakistan. The study included psychiatry residents, fellows, and consultants. A 48-item questionnaire, internally and externally validated, assessed knowledge, perceptions, and willingness to adopt digital psychiatry tools—telepsychiatry, artificial intelligence, mental health applications, and virtual reality. Data were analyzed using Statistical Package for the Social Sciences (version 26) for descriptive statistics, correlation, and regression analyses, while thematic analysis of open-ended responses was performed using Quirkos.
Results:
A total of 200 participants (56.0% aged 20–30 years, n = 112; 55.5% male, n = 111) were part of this study. 68.5% (n = 137) understood the applications of telepsychiatry, while 72.5% (n = 145) agreed that it is time-efficient and cost-effective. Only 39.5% (n = 79) of participants had received relevant artificial intelligence training to incorporate it in their psychiatric clinical practice. 62.0% (n = 124) of respondents reported unfamiliarity with the use of mental health applications. Regarding virtual reality, 32.5% (n = 65) were familiar with the technology, but only 42.5% (n = 85) were aware of its applications in psychiatric care. Thematic reflexive analysis revealed major challenges, including a ‘lack of infrastructure/resources’ (44.5%, n = 89) and a ‘lack of education/awareness’ (21.5%, n = 43).
Conclusions:
This study represents the first cross-sectional examination of digital psychiatric literacy in Pakistan’s healthcare system, which revealed significant gaps in digital health competencies among psychiatrists. Given the vast potential of emerging technologies in addressing mental health challenges, there is an urgent need for mental health professionals in Pakistan to integrate digitization in psychiatric practice.
Aim:
A comprehensive understanding of current digital literacy and perspectives of the psychiatric workforce is important to introduce appropriate digital psychiatry interventions and implement contextually relevant measures in Pakistan. This study aims to address a gap in the existing literature by assessing psychiatrists’ knowledge, attitudes, perceived barriers, and willingness to integrate digital psychiatry into their clinical practice.
Methods:
A cross-sectional online survey was conducted from January 2023 to June 2023 across psychiatric departments of 18 public hospitals in Pakistan. The study included psychiatry residents, fellows, and consultants. A 48-item questionnaire, internally and externally validated, assessed knowledge, perceptions, and willingness to adopt digital psychiatry tools—telepsychiatry, artificial intelligence, mental health applications, and virtual reality. Data were analyzed using Statistical Package for the Social Sciences (version 26) for descriptive statistics, correlation, and regression analyses, while thematic analysis of open-ended responses was performed using Quirkos.
Results:
A total of 200 participants (56.0% aged 20–30 years, n = 112; 55.5% male, n = 111) were part of this study. 68.5% (n = 137) understood the applications of telepsychiatry, while 72.5% (n = 145) agreed that it is time-efficient and cost-effective. Only 39.5% (n = 79) of participants had received relevant artificial intelligence training to incorporate it in their psychiatric clinical practice. 62.0% (n = 124) of respondents reported unfamiliarity with the use of mental health applications. Regarding virtual reality, 32.5% (n = 65) were familiar with the technology, but only 42.5% (n = 85) were aware of its applications in psychiatric care. Thematic reflexive analysis revealed major challenges, including a ‘lack of infrastructure/resources’ (44.5%, n = 89) and a ‘lack of education/awareness’ (21.5%, n = 43).
Conclusions:
This study represents the first cross-sectional examination of digital psychiatric literacy in Pakistan’s healthcare system, which revealed significant gaps in digital health competencies among psychiatrists. Given the vast potential of emerging technologies in addressing mental health challenges, there is an urgent need for mental health professionals in Pakistan to integrate digitization in psychiatric practice.
DOI: https://doi.org/10.37349/edht.2026.101179
This article belongs to the special issue Telepsychiatry in Low-and Middle-income Countries: an Update
Background:
The root cause of diabetes is dysregulated pathways, including those involving AMP-activated protein kinase (AMPK), GLUT-mediated glucose transport, and the PI3K/AKT pathway. There has been a notable increase in research on phytoconstituents as pathway-specific treatments for diabetes; however, the comprehensiveness of this evidence remains unclear.
Methods:
This systematic review followed PRISMA guidelines and was registered on PROSPERO (CRD420251073083). Databases searched included PubMed, Scopus, Google Scholar, and Europe PMC for experimental studies (in vivo, in vitro, and in silico) published between 2015 and 2024. The final search was conducted in April 2025, and 2025 publications available as “early access” before this date were included. Only English-language studies were included. Animal studies (in vivo) were assessed for risk of bias using the SYRCLE tool, while in vitro studies were evaluated using the ToxRTool, based on test substance characterization, test system description, study design, and data reporting. Narrative synthesis was employed due to the heterogeneity of the data.
Results:
Out of 3,222 articles, 177 articles met the inclusion criteria. Study types included in vitro (92; 52%), in vivo (66; 37.3%), in silico (15; 8.5%), and other experimental types (4; 2.3%). Phytoconstituents predominantly targeted PI3K/AKT (44.6%), GLUT transporters (19.8%), and AMPK (14.1%) pathways. Rodent models were most used (48.02%). Primary outcomes included improved insulin sensitivity, enhanced glucose homeostasis, and reduced oxidative stress and inflammation. The risk of bias analysis revealed 68.93% of the studies carried a moderate risk, 29.94% a low risk, and 1.13% a high risk.
Discussion:
Phytoconstituent activity was consistent with the activation of diabetes-relevant signaling pathways, particularly PI3K/AKT, GLUT transporters, and AMPK cascades. However, most evidence was correlative, with limited loss-of-function validation. Methodological irregularities, moderate risk of bias, and limited translational research reduce the strength and generalizability of these findings.
Background:
The root cause of diabetes is dysregulated pathways, including those involving AMP-activated protein kinase (AMPK), GLUT-mediated glucose transport, and the PI3K/AKT pathway. There has been a notable increase in research on phytoconstituents as pathway-specific treatments for diabetes; however, the comprehensiveness of this evidence remains unclear.
Methods:
This systematic review followed PRISMA guidelines and was registered on PROSPERO (CRD420251073083). Databases searched included PubMed, Scopus, Google Scholar, and Europe PMC for experimental studies (in vivo, in vitro, and in silico) published between 2015 and 2024. The final search was conducted in April 2025, and 2025 publications available as “early access” before this date were included. Only English-language studies were included. Animal studies (in vivo) were assessed for risk of bias using the SYRCLE tool, while in vitro studies were evaluated using the ToxRTool, based on test substance characterization, test system description, study design, and data reporting. Narrative synthesis was employed due to the heterogeneity of the data.
Results:
Out of 3,222 articles, 177 articles met the inclusion criteria. Study types included in vitro (92; 52%), in vivo (66; 37.3%), in silico (15; 8.5%), and other experimental types (4; 2.3%). Phytoconstituents predominantly targeted PI3K/AKT (44.6%), GLUT transporters (19.8%), and AMPK (14.1%) pathways. Rodent models were most used (48.02%). Primary outcomes included improved insulin sensitivity, enhanced glucose homeostasis, and reduced oxidative stress and inflammation. The risk of bias analysis revealed 68.93% of the studies carried a moderate risk, 29.94% a low risk, and 1.13% a high risk.
Discussion:
Phytoconstituent activity was consistent with the activation of diabetes-relevant signaling pathways, particularly PI3K/AKT, GLUT transporters, and AMPK cascades. However, most evidence was correlative, with limited loss-of-function validation. Methodological irregularities, moderate risk of bias, and limited translational research reduce the strength and generalizability of these findings.
DOI: https://doi.org/10.37349/eds.2026.1008139
Artificial intelligence (AI) is transforming healthcare by equipping clinicians and patients with tools that support more efficient, patient-centered care. In pediatrics, however, the implementation of AI demands a higher threshold for responsibility, transparency, and family-centered engagement. This perspective explores the opportunities and challenges of AI in pediatric healthcare, highlighting the unique ethical and developmental considerations that distinguish children’s care from adult medicine. Drawing on Kaiser Permanente’s seven principles for responsible AI, the article emphasizes the importance of augmentation over automation, the need for pediatric-specific validation, and the necessity of trustworthiness and fairness in clinical deployment. It outlines how AI can support primary care providers through enhanced decision support, early screening for developmental and behavioral disorders, including the potential for AI to create personalized developmental trajectories, moving beyond static population norms to provide earlier, more precise insights into a child’s neurodevelopmental progress, improved electronic health record usability, and risk prediction models. However, without careful governance, AI poses risks of bias, inequity, and erosion of clinician judgment. Policy recommendations include redesigning family consent models, ensuring robust clinician training, and mandating pediatric-specific testing of AI systems with diverse, representative datasets. Ultimately, AI should function as a supportive tool that strengthens, not replaces, human empathy, clinical expertise, and family-centered values. Responsible innovation is essential to ensure that children benefit equitably from AI while maintaining trust, safety, and compassion in pediatric healthcare.
Artificial intelligence (AI) is transforming healthcare by equipping clinicians and patients with tools that support more efficient, patient-centered care. In pediatrics, however, the implementation of AI demands a higher threshold for responsibility, transparency, and family-centered engagement. This perspective explores the opportunities and challenges of AI in pediatric healthcare, highlighting the unique ethical and developmental considerations that distinguish children’s care from adult medicine. Drawing on Kaiser Permanente’s seven principles for responsible AI, the article emphasizes the importance of augmentation over automation, the need for pediatric-specific validation, and the necessity of trustworthiness and fairness in clinical deployment. It outlines how AI can support primary care providers through enhanced decision support, early screening for developmental and behavioral disorders, including the potential for AI to create personalized developmental trajectories, moving beyond static population norms to provide earlier, more precise insights into a child’s neurodevelopmental progress, improved electronic health record usability, and risk prediction models. However, without careful governance, AI poses risks of bias, inequity, and erosion of clinician judgment. Policy recommendations include redesigning family consent models, ensuring robust clinician training, and mandating pediatric-specific testing of AI systems with diverse, representative datasets. Ultimately, AI should function as a supportive tool that strengthens, not replaces, human empathy, clinical expertise, and family-centered values. Responsible innovation is essential to ensure that children benefit equitably from AI while maintaining trust, safety, and compassion in pediatric healthcare.
DOI: https://doi.org/10.37349/edht.2026.101178
This article belongs to the special issue Expert Opinions on Digital Health Innovations
Aim:
This study aimed to establish the in vitro efficacy of chlorhexidine (CHX)-silver nanoparticles (AgNP) based preparation, against Staphylococcus aureus (S. aureus) and Pseudomonas aeruginosa (P. aeruginosa) in planktonic cultures, biofilms, and on inert stainless-steel surfaces.
Methods:
The in vitro antimicrobial activity of the CHX-AgNP formulation (Dermosedan MRSA Nano AG®) was evaluated against reference and multidrug-resistant (MDR) strains of S. aureus and P. aeruginosa by determining the minimum inhibitory and bactericidal concentrations (MIC and MBC), as well as the minimum biofilm inhibitory and eradication concentrations (MBIC and MBEC). Also, the residual bactericidal activity on inert stainless-steel surfaces was evaluated.
Results:
MIC against methicillin-resistant S. aureus (MRSA) and MDR P. aeruginosa (MDR-PA) isolates ranged between 5/2.5–20/10 µg/mL, up to 8,000 times lower than the manufacturer’s recommended concentration, while MBC ranged from 500 to 2,000 times lower. MBIC matched the MBC, while higher concentrations were needed to eradicate preformed biofilms. On stainless-steel surfaces, high antimicrobial activity was observed for both pathogens. No bacterial survival was detected even after 6 hours at 4% CHX + 2% AgNP concentration. The CHX-AgNP combination demonstrated strong antimicrobial and antibiofilm activity against both S. aureus and P. aeruginosa.
Conclusions:
These results support the potential application of Dermosedan MRSA Nano AG® as a strategy for managing topical resistant infections and for environmental disinfection in both veterinary and clinical settings.
Aim:
This study aimed to establish the in vitro efficacy of chlorhexidine (CHX)-silver nanoparticles (AgNP) based preparation, against Staphylococcus aureus (S. aureus) and Pseudomonas aeruginosa (P. aeruginosa) in planktonic cultures, biofilms, and on inert stainless-steel surfaces.
Methods:
The in vitro antimicrobial activity of the CHX-AgNP formulation (Dermosedan MRSA Nano AG®) was evaluated against reference and multidrug-resistant (MDR) strains of S. aureus and P. aeruginosa by determining the minimum inhibitory and bactericidal concentrations (MIC and MBC), as well as the minimum biofilm inhibitory and eradication concentrations (MBIC and MBEC). Also, the residual bactericidal activity on inert stainless-steel surfaces was evaluated.
Results:
MIC against methicillin-resistant S. aureus (MRSA) and MDR P. aeruginosa (MDR-PA) isolates ranged between 5/2.5–20/10 µg/mL, up to 8,000 times lower than the manufacturer’s recommended concentration, while MBC ranged from 500 to 2,000 times lower. MBIC matched the MBC, while higher concentrations were needed to eradicate preformed biofilms. On stainless-steel surfaces, high antimicrobial activity was observed for both pathogens. No bacterial survival was detected even after 6 hours at 4% CHX + 2% AgNP concentration. The CHX-AgNP combination demonstrated strong antimicrobial and antibiofilm activity against both S. aureus and P. aeruginosa.
Conclusions:
These results support the potential application of Dermosedan MRSA Nano AG® as a strategy for managing topical resistant infections and for environmental disinfection in both veterinary and clinical settings.
DOI: https://doi.org/10.37349/eds.2026.1008138
This article belongs to the special issue Discovery and development of new antibacterial compounds
Pulmonary embolism (PE) is the third most common cause of cardiovascular mortality and presents a significant challenge in acute care settings. EkoSonic Endovascular System (EKOS) (ultrasound assisted catheter directed thrombolysis) and suction thrombectomy have emerged as key treatment options for high and intermediate risk PE. EKOS delivers localized fibrinolytic therapy, whereas thrombectomy provides definitive clot removal using devices such as the FlowTriever System (Inari Medical). However, the optimal treatment strategy, particularly in recurrent PE, remains uncertain. We report a case requiring escalation of therapy from EKOS to suction thrombectomy due to recurrent PE and worsening hemodynamic status despite initial thrombolysis. The patient was initially treated with EKOS for a saddle PE but was rehospitalized with syncope and persistent right ventricular (RV) strain. Given the inadequate response to thrombolysis, suction thrombectomy was performed, leading to marked improvement in RV function and overall clinical status. This case underscores the importance of individualized management and timely escalation when initial therapy is insufficient. Assessment of therapeutic success should include not only symptomatic relief but also resolution of clot burden and RV recovery. A focused literature review comparing EKOS and suction thrombectomy suggests that while both modalities are viable, suction thrombectomy may offer faster hemodynamic improvement in select patients. However, available data remains limited, highlighting the need for further comparative studies. Overall, this case and review support a tailored, multidisciplinary approach to PE management, emphasizing shared decision making and early escalation in patients with clinical deterioration despite initial intervention.
Pulmonary embolism (PE) is the third most common cause of cardiovascular mortality and presents a significant challenge in acute care settings. EkoSonic Endovascular System (EKOS) (ultrasound assisted catheter directed thrombolysis) and suction thrombectomy have emerged as key treatment options for high and intermediate risk PE. EKOS delivers localized fibrinolytic therapy, whereas thrombectomy provides definitive clot removal using devices such as the FlowTriever System (Inari Medical). However, the optimal treatment strategy, particularly in recurrent PE, remains uncertain. We report a case requiring escalation of therapy from EKOS to suction thrombectomy due to recurrent PE and worsening hemodynamic status despite initial thrombolysis. The patient was initially treated with EKOS for a saddle PE but was rehospitalized with syncope and persistent right ventricular (RV) strain. Given the inadequate response to thrombolysis, suction thrombectomy was performed, leading to marked improvement in RV function and overall clinical status. This case underscores the importance of individualized management and timely escalation when initial therapy is insufficient. Assessment of therapeutic success should include not only symptomatic relief but also resolution of clot burden and RV recovery. A focused literature review comparing EKOS and suction thrombectomy suggests that while both modalities are viable, suction thrombectomy may offer faster hemodynamic improvement in select patients. However, available data remains limited, highlighting the need for further comparative studies. Overall, this case and review support a tailored, multidisciplinary approach to PE management, emphasizing shared decision making and early escalation in patients with clinical deterioration despite initial intervention.
DOI: https://doi.org/10.37349/ec.2026.101285
