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Pollen-related allergic diseases, including allergic rhinoconjunctivitis and asthma, affect a growing proportion of the population and have substantial consequences for quality of life and healthcare systems. Conventional pollen forecasts, which rely on fixed pollen traps and meteorological data, are limited in spatial granularity, real-time responsiveness, and individual relevance. Recent advances in artificial intelligence (AI) and machine learning (ML) offer a paradigm shift in the modelling of pollen release, forecast exposure, and alert allergic patients. This article provides a comprehensive overview of ML-based pollen forecasting systems, clarifying their underlying principles in accessible terms for clinicians and presenting practical and published tools that allergologists can integrate into routine practice. By combining aerobiological data, meteorological models, and patient-reported outcomes, ML enables more personalized, precise, and timely allergy management. We review the fundamental mechanisms of pollen release and dispersion and illustrate how ML models can improve predictive accuracy. Key platforms are compared in terms of clinical usability. We present real-world use cases showing how ML-driven alerts can help optimize treatment plans and support patient education. Practical insights are provided on the evaluation, implementation, and limitations of these tools. ML is not a distant technology—it is already transforming pollen forecasting and allergy alerts. This article aims to equip allergologists with the knowledge needed to evaluate and adopt these tools, enabling a more proactive and personalized approach to managing pollen allergies.
Pollen-related allergic diseases, including allergic rhinoconjunctivitis and asthma, affect a growing proportion of the population and have substantial consequences for quality of life and healthcare systems. Conventional pollen forecasts, which rely on fixed pollen traps and meteorological data, are limited in spatial granularity, real-time responsiveness, and individual relevance. Recent advances in artificial intelligence (AI) and machine learning (ML) offer a paradigm shift in the modelling of pollen release, forecast exposure, and alert allergic patients. This article provides a comprehensive overview of ML-based pollen forecasting systems, clarifying their underlying principles in accessible terms for clinicians and presenting practical and published tools that allergologists can integrate into routine practice. By combining aerobiological data, meteorological models, and patient-reported outcomes, ML enables more personalized, precise, and timely allergy management. We review the fundamental mechanisms of pollen release and dispersion and illustrate how ML models can improve predictive accuracy. Key platforms are compared in terms of clinical usability. We present real-world use cases showing how ML-driven alerts can help optimize treatment plans and support patient education. Practical insights are provided on the evaluation, implementation, and limitations of these tools. ML is not a distant technology—it is already transforming pollen forecasting and allergy alerts. This article aims to equip allergologists with the knowledge needed to evaluate and adopt these tools, enabling a more proactive and personalized approach to managing pollen allergies.
DOI: https://doi.org/10.37349/eaa.2026.1009123
This article belongs to the special issue Climate Change, Allergy, and Immunotherapy
Major depressive disorder (MDD) is increasingly understood as a multifactorial psychiatric disorder involving interacting neural, immune, metabolic, and microbial processes. Within this framework, the microbiota–gut–brain axis and mitochondrial bioenergetics have emerged as potentially intersecting contributors to depressive symptomatology. Preclinical studies suggest that microbial metabolites—especially short-chain fatty acids (SCFAs)—can influence oxidative phosphorylation, redox balance, neuroinflammation, and synaptic plasticity, whereas inflammatory signals such as lipopolysaccharide may disrupt mitochondrial dynamics. However, the strength of evidence is uneven: mechanistic support is strongest in cell and animal models, whereas human data remain heterogeneous and largely associative. This narrative review critically synthesizes current evidence on microbiota–mitochondria crosstalk in MDD, distinguishing established findings from emerging hypotheses. It also examines recent psychobiotic trials, metabolomic and biomarker studies, and microglia–mitochondria mechanisms, and discusses the translational limitations that currently constrain clinical application. Overall, this axis represents a plausible and clinically relevant framework for hypothesis generation and adjunctive intervention development, but it should not yet be regarded as a fully validated causal pathway or stand-alone therapeutic target in MDD.
Major depressive disorder (MDD) is increasingly understood as a multifactorial psychiatric disorder involving interacting neural, immune, metabolic, and microbial processes. Within this framework, the microbiota–gut–brain axis and mitochondrial bioenergetics have emerged as potentially intersecting contributors to depressive symptomatology. Preclinical studies suggest that microbial metabolites—especially short-chain fatty acids (SCFAs)—can influence oxidative phosphorylation, redox balance, neuroinflammation, and synaptic plasticity, whereas inflammatory signals such as lipopolysaccharide may disrupt mitochondrial dynamics. However, the strength of evidence is uneven: mechanistic support is strongest in cell and animal models, whereas human data remain heterogeneous and largely associative. This narrative review critically synthesizes current evidence on microbiota–mitochondria crosstalk in MDD, distinguishing established findings from emerging hypotheses. It also examines recent psychobiotic trials, metabolomic and biomarker studies, and microglia–mitochondria mechanisms, and discusses the translational limitations that currently constrain clinical application. Overall, this axis represents a plausible and clinically relevant framework for hypothesis generation and adjunctive intervention development, but it should not yet be regarded as a fully validated causal pathway or stand-alone therapeutic target in MDD.
DOI: https://doi.org/10.37349/en.2026.1006133
This article belongs to the special issue Depression: From Pathophysiology to Treatment Innovation
Aim:
This study aimed to determine the best formulation of gluten-free biscuits made from red rice and cassava composite flour and to evaluate their physicochemical properties, shelf life, and consumer acceptability.
Methods:
Five biscuit formulations (F1: 100:0, F2: 75:25, F3: 50:50, F4: 25:75, F5: 0:100; red rice flour:cassava flour) were prepared. Sensory evaluation using a nine-point hedonic scale identified the optimal formulation. The selected biscuit was further analyzed for proximate composition, dietary fiber, total energy, and physical properties (hardness, color, spread ratio, and bulk density). Shelf life was monitored over eight weeks through microbiological counts, water activity, and texture changes. Consumer acceptance was assessed via a market survey.
Results:
F3 (50:50) achieved the highest scores for color, aroma, taste, crispiness, and overall acceptance. It contained lower moisture (2.87%) and protein (5.45%) but higher ash (0.81%), carbohydrate (72.46%), dietary fiber (3.57%), and energy (474.03 kcal/100 g) than the control (p < 0.05). Fat and crude fiber contents did not differ significantly among the formulations (p > 0.05). F3 showed lower hardness, darker color, higher spread ratio, and greater bulk density. Microbial counts remained at < 10 CFU g⁻1 and water activity ≤ 0.65 during storage, while hardness gradually decreased. Over 70% of consumers rated the product as highly acceptable.
Conclusions:
A 50:50 red rice-cassava formulation produced gluten-free biscuits with favorable nutritional, physical, and sensory qualities and good storage stability, indicating strong potential as a functional snack product.
Aim:
This study aimed to determine the best formulation of gluten-free biscuits made from red rice and cassava composite flour and to evaluate their physicochemical properties, shelf life, and consumer acceptability.
Methods:
Five biscuit formulations (F1: 100:0, F2: 75:25, F3: 50:50, F4: 25:75, F5: 0:100; red rice flour:cassava flour) were prepared. Sensory evaluation using a nine-point hedonic scale identified the optimal formulation. The selected biscuit was further analyzed for proximate composition, dietary fiber, total energy, and physical properties (hardness, color, spread ratio, and bulk density). Shelf life was monitored over eight weeks through microbiological counts, water activity, and texture changes. Consumer acceptance was assessed via a market survey.
Results:
F3 (50:50) achieved the highest scores for color, aroma, taste, crispiness, and overall acceptance. It contained lower moisture (2.87%) and protein (5.45%) but higher ash (0.81%), carbohydrate (72.46%), dietary fiber (3.57%), and energy (474.03 kcal/100 g) than the control (p < 0.05). Fat and crude fiber contents did not differ significantly among the formulations (p > 0.05). F3 showed lower hardness, darker color, higher spread ratio, and greater bulk density. Microbial counts remained at < 10 CFU g⁻1 and water activity ≤ 0.65 during storage, while hardness gradually decreased. Over 70% of consumers rated the product as highly acceptable.
Conclusions:
A 50:50 red rice-cassava formulation produced gluten-free biscuits with favorable nutritional, physical, and sensory qualities and good storage stability, indicating strong potential as a functional snack product.
DOI: https://doi.org/10.37349/eff.2026.1010136
Obesity is a determinant of the risk of developing various diseases, including asthma. It can also contribute to asthma severity. Obvious determinants of the risk of developing obesity and conditions associated with obesity are the diet an individual consumes and their energy expenditure, as determined by activity. Therefore, diet and exercise are important non-pharmacological components in the management and prevention of many diseases. Several individual elements in diet, including certain fatty acids and vitamins, as well as types of diets, notably the Mediterranean diet, have been studied in asthmatic patients, but the literature is not consistent. This review explores the relationship between asthma and obesity, exercise, and multiple dietary components and regimens, including the Mediterranean diet; polyunsaturated fats; vitamins A, C, D, and E; flavonoids; probiotics; and sodium intake in the published randomized clinical trials. Overall, the data have many shortcomings, but there is no single component of diet that is consistently associated with improved asthma outcomes, nor any component found to be clearly harmful. However, a diet that helps an individual lose weight may indirectly improve their lung function and asthma control, even if the diet itself does not impact asthma outcomes. Exercise, now known to be safe and widely recommended in asthma, has various forms. This review looked at meta-analyses, as well as recently published data addressing this question, categorizing exercise as aerobic activity, pulmonary rehabilitation, and yoga. The most evidence for benefit is for aerobic exercise, but yoga also has potential for modest improvement in asthma symptoms. There is conflicting data as to whether supervised exercise programs are superior to unsupervised physical activity. Overall, exercise is helpful in asthma, but it is still unclear how much exercise should be done, and this should be tailored to each individual.
Obesity is a determinant of the risk of developing various diseases, including asthma. It can also contribute to asthma severity. Obvious determinants of the risk of developing obesity and conditions associated with obesity are the diet an individual consumes and their energy expenditure, as determined by activity. Therefore, diet and exercise are important non-pharmacological components in the management and prevention of many diseases. Several individual elements in diet, including certain fatty acids and vitamins, as well as types of diets, notably the Mediterranean diet, have been studied in asthmatic patients, but the literature is not consistent. This review explores the relationship between asthma and obesity, exercise, and multiple dietary components and regimens, including the Mediterranean diet; polyunsaturated fats; vitamins A, C, D, and E; flavonoids; probiotics; and sodium intake in the published randomized clinical trials. Overall, the data have many shortcomings, but there is no single component of diet that is consistently associated with improved asthma outcomes, nor any component found to be clearly harmful. However, a diet that helps an individual lose weight may indirectly improve their lung function and asthma control, even if the diet itself does not impact asthma outcomes. Exercise, now known to be safe and widely recommended in asthma, has various forms. This review looked at meta-analyses, as well as recently published data addressing this question, categorizing exercise as aerobic activity, pulmonary rehabilitation, and yoga. The most evidence for benefit is for aerobic exercise, but yoga also has potential for modest improvement in asthma symptoms. There is conflicting data as to whether supervised exercise programs are superior to unsupervised physical activity. Overall, exercise is helpful in asthma, but it is still unclear how much exercise should be done, and this should be tailored to each individual.
DOI: https://doi.org/10.37349/eaa.2026.1009124
This article belongs to the special issue The Complex Interactions Between Lifestyles and Asthma
Background:
Atrial fibrillation (AF) substantially increases the risk of ischemic stroke (IS), underscoring the need for effective anticoagulation strategies. Direct oral anticoagulants (DOACs) have largely supplanted vitamin K antagonists (VKAs) due to their favorable safety profile and ease of use. Factor XI (FXI) inhibitors, which target the intrinsic coagulation pathway, are emerging as potential alternatives that may offer reduced bleeding risk. This systematic review evaluates the efficacy and safety of FXI inhibitors compared with DOACs for stroke prevention in AF.
Methods:
A total of 20 studies fulfilled the inclusion criteria, comprising 11 randomized controlled trials (RCTs), five systematic reviews or meta-analyses, and four narrative, cohort, or modeling studies. Eligible investigations compared FXI inhibitors with DOACs in patients diagnosed with AF. The primary outcomes assessed were stroke or systemic embolism, major bleeding, and all-cause mortality. Methodological quality was evaluated according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) framework, the revised Cochrane Risk of Bias 2 (RoB 2) tool for RCTs, and the Newcastle-Ottawa Scale (NOS).
Results:
FXI inhibitors were associated with a significant reduction in major bleeding [relative risk (RR) 0.31; 95% confidence interval (CI) 0.21–0.46] and clinically relevant non-major bleeding (RR 0.66; 95% CI 0.47–0.93) compared with DOACs. Conversely, FXI inhibitors demonstrated an increased risk of stroke or systemic embolism (RR 3.17; 95% CI 2.18–4.62), as observed in the OCEANIC-AF trial [hazard ratio (HR) 3.79; 95% CI 2.46–5.83]. No significant difference was noted in all-cause mortality (RR 0.85; 95% CI 0.67–1.08). Limited evidence suggests that FXI inhibitors may also reduce bleeding-related hospitalizations.
Discussion:
FXI inhibitors provide a favorable bleeding profile but are less effective than DOACs for stroke prevention in patients with AF. Further long-term RCTs are warranted to delineate their role, particularly in populations at high risk of bleeding.
Background:
Atrial fibrillation (AF) substantially increases the risk of ischemic stroke (IS), underscoring the need for effective anticoagulation strategies. Direct oral anticoagulants (DOACs) have largely supplanted vitamin K antagonists (VKAs) due to their favorable safety profile and ease of use. Factor XI (FXI) inhibitors, which target the intrinsic coagulation pathway, are emerging as potential alternatives that may offer reduced bleeding risk. This systematic review evaluates the efficacy and safety of FXI inhibitors compared with DOACs for stroke prevention in AF.
Methods:
A total of 20 studies fulfilled the inclusion criteria, comprising 11 randomized controlled trials (RCTs), five systematic reviews or meta-analyses, and four narrative, cohort, or modeling studies. Eligible investigations compared FXI inhibitors with DOACs in patients diagnosed with AF. The primary outcomes assessed were stroke or systemic embolism, major bleeding, and all-cause mortality. Methodological quality was evaluated according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) framework, the revised Cochrane Risk of Bias 2 (RoB 2) tool for RCTs, and the Newcastle-Ottawa Scale (NOS).
Results:
FXI inhibitors were associated with a significant reduction in major bleeding [relative risk (RR) 0.31; 95% confidence interval (CI) 0.21–0.46] and clinically relevant non-major bleeding (RR 0.66; 95% CI 0.47–0.93) compared with DOACs. Conversely, FXI inhibitors demonstrated an increased risk of stroke or systemic embolism (RR 3.17; 95% CI 2.18–4.62), as observed in the OCEANIC-AF trial [hazard ratio (HR) 3.79; 95% CI 2.46–5.83]. No significant difference was noted in all-cause mortality (RR 0.85; 95% CI 0.67–1.08). Limited evidence suggests that FXI inhibitors may also reduce bleeding-related hospitalizations.
Discussion:
FXI inhibitors provide a favorable bleeding profile but are less effective than DOACs for stroke prevention in patients with AF. Further long-term RCTs are warranted to delineate their role, particularly in populations at high risk of bleeding.
DOI: https://doi.org/10.37349/ent.2026.1004148
This article belongs to the special issue Interdisciplinary Approach to Therapeutic Strategies of Neuroprotection in Present and Future
Aim:
To evaluate the relationship between serum calprotectin and serum amyloid A with musculoskeletal ultrasonographic findings in rheumatoid arthritis (RA) patients, as RA is the most common chronic inflammatory joint disease in which the infiltration and activation of inflammatory cells are important. Calprotectin and serum amyloid A protein are over-secreted in response to acute and chronic inflammation. Musculoskeletal ultrasound is more sensitive than physical examination for the evaluation of synovitis.
Methods:
A control group of 30 healthy individuals, 30 patients with active RA, and 30 patients with inactive RA participated in this cross-sectional study. Utilizing the RA disease activity (Disease Activity Score 28, DAS28) score was evaluated. Serum amyloid A and serum calprotectin were measured in all participants, and musculoskeletal ultrasound on the hands and wrists were done for all subjects.
Results:
A significant difference was observed among the studied groups with respect to serum calprotectin and serum amyloid A levels (P < 0.001). A significant positive correlation was observed between serum amyloid A and several inflammatory and clinical parameters, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), DAS28 score, serum calprotectin, and synovitis. Similarly, serum calprotectin levels demonstrated a significant positive correlation with ESR, DAS28 score, serum amyloid A, and synovitis. These findings highlight the potential value of both serum amyloid A and serum calprotectin as biomarkers reflecting disease activity and inflammatory burden in RA.
Conclusions:
Serum amyloid A and serum calprotectin can be used as markers of RA activity.
Aim:
To evaluate the relationship between serum calprotectin and serum amyloid A with musculoskeletal ultrasonographic findings in rheumatoid arthritis (RA) patients, as RA is the most common chronic inflammatory joint disease in which the infiltration and activation of inflammatory cells are important. Calprotectin and serum amyloid A protein are over-secreted in response to acute and chronic inflammation. Musculoskeletal ultrasound is more sensitive than physical examination for the evaluation of synovitis.
Methods:
A control group of 30 healthy individuals, 30 patients with active RA, and 30 patients with inactive RA participated in this cross-sectional study. Utilizing the RA disease activity (Disease Activity Score 28, DAS28) score was evaluated. Serum amyloid A and serum calprotectin were measured in all participants, and musculoskeletal ultrasound on the hands and wrists were done for all subjects.
Results:
A significant difference was observed among the studied groups with respect to serum calprotectin and serum amyloid A levels (P < 0.001). A significant positive correlation was observed between serum amyloid A and several inflammatory and clinical parameters, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), DAS28 score, serum calprotectin, and synovitis. Similarly, serum calprotectin levels demonstrated a significant positive correlation with ESR, DAS28 score, serum amyloid A, and synovitis. These findings highlight the potential value of both serum amyloid A and serum calprotectin as biomarkers reflecting disease activity and inflammatory burden in RA.
Conclusions:
Serum amyloid A and serum calprotectin can be used as markers of RA activity.
DOI: https://doi.org/10.37349/ei.2026.1003249
Recurrent infections in children often prompt evaluation for primary immunodeficiency diseases, particularly those affecting humoral immunity. Assessment of memory B cell subsets and vaccine-specific antibody responses provides critical insight into long-term protective immunity. While peripheral blood mononuclear cell (PBMC) isolation is common, direct whole blood staining offers faster processing, reduced cell loss, and better preservation of fragile B cell populations. This comprehensive protocol describes a standardised whole blood flow cytometry method for memory B cell phenotyping, alongside ELISA-based measurement of vaccine-specific antibody titres as part of assessing children with recurrent infections.
Recurrent infections in children often prompt evaluation for primary immunodeficiency diseases, particularly those affecting humoral immunity. Assessment of memory B cell subsets and vaccine-specific antibody responses provides critical insight into long-term protective immunity. While peripheral blood mononuclear cell (PBMC) isolation is common, direct whole blood staining offers faster processing, reduced cell loss, and better preservation of fragile B cell populations. This comprehensive protocol describes a standardised whole blood flow cytometry method for memory B cell phenotyping, alongside ELISA-based measurement of vaccine-specific antibody titres as part of assessing children with recurrent infections.
DOI: https://doi.org/10.37349/ei.2026.1003248
Background:
Sickle cell disease (SCD) is a group of heritable conditions with significant morbidity, burden of disease management and healthcare delivery issues. Medical mistrust (MM) is a psychological outcome of healthcare delivery issues. The purpose of this review was to assess the concept of MM in the literature on SCD, summarize the findings and gaps, and was guided by three questions: 1) How has MM been measured and/or described in patients with SCD? 2) What factors have been described in the literature that predispose patients with SCD to develop MM? 3) What consequences or outcomes have been described because of MM in patients with SCD?
Methods:
The methodological framework of Arksey and O’Malley was used to review articles from PubMed, Scopus, Web of Science, CINAHL, PsycInfo, and EMBASE. Inclusion criteria were quantitative, qualitative, and mixed methods peer-reviewed studies published in English between 1994 and 2025; articles focused on patients with SCD and those that described concepts found in the existing MM instruments.
Results:
Forty-two studies were included; 26 were strictly qualitative, 11 were mixed methods, and 5 were strictly quantitative. No study used an existing MM measure; yet concepts from MM measures were described: group disparities and suspicion. Negative healthcare staff communication, poor pain control, transition of care, and lack of provider transparency predisposed patients toward MM. Outcomes of MM included avoidance of care, nonadherence, psychological distress, and maladaptive coping.
Discussion:
This review highlights the predictors and outcomes of MM in patients with SCD and identifies the notable gaps in the state of the SCD MM literature. More studies are needed to assess the development and consequences of MM in patients with SCD. The findings highlight the experiences of patients with SCD and offer researchers insights into possible interventions to decrease MM and improve outcomes.
Background:
Sickle cell disease (SCD) is a group of heritable conditions with significant morbidity, burden of disease management and healthcare delivery issues. Medical mistrust (MM) is a psychological outcome of healthcare delivery issues. The purpose of this review was to assess the concept of MM in the literature on SCD, summarize the findings and gaps, and was guided by three questions: 1) How has MM been measured and/or described in patients with SCD? 2) What factors have been described in the literature that predispose patients with SCD to develop MM? 3) What consequences or outcomes have been described because of MM in patients with SCD?
Methods:
The methodological framework of Arksey and O’Malley was used to review articles from PubMed, Scopus, Web of Science, CINAHL, PsycInfo, and EMBASE. Inclusion criteria were quantitative, qualitative, and mixed methods peer-reviewed studies published in English between 1994 and 2025; articles focused on patients with SCD and those that described concepts found in the existing MM instruments.
Results:
Forty-two studies were included; 26 were strictly qualitative, 11 were mixed methods, and 5 were strictly quantitative. No study used an existing MM measure; yet concepts from MM measures were described: group disparities and suspicion. Negative healthcare staff communication, poor pain control, transition of care, and lack of provider transparency predisposed patients toward MM. Outcomes of MM included avoidance of care, nonadherence, psychological distress, and maladaptive coping.
Discussion:
This review highlights the predictors and outcomes of MM in patients with SCD and identifies the notable gaps in the state of the SCD MM literature. More studies are needed to assess the development and consequences of MM in patients with SCD. The findings highlight the experiences of patients with SCD and offer researchers insights into possible interventions to decrease MM and improve outcomes.
DOI: https://doi.org/10.37349/emed.2026.1001400
The involvement of the Internet of Things (IoT) technology and artificial intelligence (AI) in the matter of maternal healthcare has allowed monitoring pregnant women in real-time and predicting poor pregnancy outcomes, including stillbirth and premature birth. Nevertheless, to diminish the risks of devices, the introduction of such technologies has to be accompanied by harsh safety monitoring programs. Materiovigilance, as the systematic sensing and monitoring of adverse events associated with medical instruments, is also crucial to patient safety in high-risk obstetric environments. Wearable sensors, e.g., fetal Dopplers, smart fabrics, and adhesive patches, have enhanced the prediction of stillbirth by offering continuous acquisition of physiological data but presents a hazard of ill effects if not controlled adequately. The AI introduction into the sphere of Materiovigilance enhances regulatory conformity, real-time decision-making, and raises the possibility of risk identification. Despite the massive potential, issues such as inaccurate data, poor infrastructure, and underreporting persist, particularly in low- and middle-income countries. In such circumstances, the Materiovigilance Programme of India is another staged effort to enhance the device safety supervision and reporting systems. Engagement of different stakeholders such as clinicians, engineers, regulatory agencies, and technology developers provides an opportunity to secure the safety and efficacy of AI-equipped medical devices. Enhancement of Materiovigilance systems is required to preserve proper maternal-fetal health and sustain clinics in digital obstetrics, as any error in maternal-fetal monitoring may lead to preventable death.
The involvement of the Internet of Things (IoT) technology and artificial intelligence (AI) in the matter of maternal healthcare has allowed monitoring pregnant women in real-time and predicting poor pregnancy outcomes, including stillbirth and premature birth. Nevertheless, to diminish the risks of devices, the introduction of such technologies has to be accompanied by harsh safety monitoring programs. Materiovigilance, as the systematic sensing and monitoring of adverse events associated with medical instruments, is also crucial to patient safety in high-risk obstetric environments. Wearable sensors, e.g., fetal Dopplers, smart fabrics, and adhesive patches, have enhanced the prediction of stillbirth by offering continuous acquisition of physiological data but presents a hazard of ill effects if not controlled adequately. The AI introduction into the sphere of Materiovigilance enhances regulatory conformity, real-time decision-making, and raises the possibility of risk identification. Despite the massive potential, issues such as inaccurate data, poor infrastructure, and underreporting persist, particularly in low- and middle-income countries. In such circumstances, the Materiovigilance Programme of India is another staged effort to enhance the device safety supervision and reporting systems. Engagement of different stakeholders such as clinicians, engineers, regulatory agencies, and technology developers provides an opportunity to secure the safety and efficacy of AI-equipped medical devices. Enhancement of Materiovigilance systems is required to preserve proper maternal-fetal health and sustain clinics in digital obstetrics, as any error in maternal-fetal monitoring may lead to preventable death.
DOI: https://doi.org/10.37349/emed.2026.1001399
Coronary vasospasm, affecting both epicardial arteries and the coronary microcirculation, is a significant yet frequently underdiagnosed and undertreated cause of coronary syndromes. When promptly identified, it carries a relatively benign prognosis. Recognition can be straightforward in non-cardiology settings when triggered by known spasmogenic agents such as misoprostol (obstetrics) or 5-fluorouracil (oncology). Vasospasm may also be incidentally revealed during noninvasive functional testing, typically presenting as ST-segment elevation during early recovery phases, or after administration of agents like aminophylline following dipyridamole or β-blockers following dobutamine. In patients with high clinical suspicion but negative Holter or stress test findings, targeted provocation with ergonovine or hyperventilation protocols can safely induce vasospasm and unmask regional wall motion abnormalities, indicating epicardial involvement. Hyperventilation-Doppler echocardiography enables the detection of microvascular dysfunction through reductions in coronary flow velocity in the mid-distal left anterior descending coronary artery. A multi-stress, multi-marker functional testing approach offers a noninvasive, safe, and effective diagnostic strategy. Inducible wall motion abnormalities are specific for epicardial spasm, while Doppler-detected flow reduction is more sensitive for microvascular dysfunction. Early diagnosis is essential, as coronary vasospasm, though potentially life-threatening, is highly manageable with appropriate therapy. Management of patients with proven epicardial coronary artery or microvascular vasospasm involves starting therapy with calcium channel blockers and nitrates, and avoiding β-blockers, as they can worsen vasospasm by blocking β2-mediated vasodilation and leaving α1-mediated vasoconstriction unopposed.
Coronary vasospasm, affecting both epicardial arteries and the coronary microcirculation, is a significant yet frequently underdiagnosed and undertreated cause of coronary syndromes. When promptly identified, it carries a relatively benign prognosis. Recognition can be straightforward in non-cardiology settings when triggered by known spasmogenic agents such as misoprostol (obstetrics) or 5-fluorouracil (oncology). Vasospasm may also be incidentally revealed during noninvasive functional testing, typically presenting as ST-segment elevation during early recovery phases, or after administration of agents like aminophylline following dipyridamole or β-blockers following dobutamine. In patients with high clinical suspicion but negative Holter or stress test findings, targeted provocation with ergonovine or hyperventilation protocols can safely induce vasospasm and unmask regional wall motion abnormalities, indicating epicardial involvement. Hyperventilation-Doppler echocardiography enables the detection of microvascular dysfunction through reductions in coronary flow velocity in the mid-distal left anterior descending coronary artery. A multi-stress, multi-marker functional testing approach offers a noninvasive, safe, and effective diagnostic strategy. Inducible wall motion abnormalities are specific for epicardial spasm, while Doppler-detected flow reduction is more sensitive for microvascular dysfunction. Early diagnosis is essential, as coronary vasospasm, though potentially life-threatening, is highly manageable with appropriate therapy. Management of patients with proven epicardial coronary artery or microvascular vasospasm involves starting therapy with calcium channel blockers and nitrates, and avoiding β-blockers, as they can worsen vasospasm by blocking β2-mediated vasodilation and leaving α1-mediated vasoconstriction unopposed.
DOI: https://doi.org/10.37349/ec.2026.1012103
Aim:
The study aimed to develop feta-type cheese from camel milk and evaluate its physicochemical properties and sensory acceptability.
Methods:
Milk samples were obtained from dromedary camels (Camelus dromedarius) kept at the Tsabong Ecotourism Camel Park in Botswana. Feta-type cheese was developed using WhiteDaily 41 culture, which contains mesophilic and thermophilic lactic acid bacteria, and camel chymosin (CHY-MAX M1000). Standard procedures were used to assess physicochemical characteristics and sensory-based consumer acceptability. Cow-milk feta cheese produced using the same procedure served as the control. Mann–Whitney test was used to compare quality parameters of the camel- and cow-milk cheeses.
Results:
The results showed that producing feta-type cheese from camel milk was more difficult than from cow milk, and the yield from camel milk was slightly lower. Except for ash and fat content, no significant differences (p > 0.05) were found between the two cheese types. Cow-milk feta had significantly higher ash and fat levels (p < 0.05) than camel-milk feta. Overall, camel-milk feta displayed physicochemical characteristics comparable to those of cow-milk feta. The sensory acceptability test revealed that aroma, texture, taste, and overall acceptability scores were significantly higher (p < 0.05) for cow-milk feta than for camel-milk feta. However, colour did not differ significantly (p > 0.05) between the two cheeses.
Conclusions:
The findings show that making feta-type cheese from camel milk is possible, provided that manufacturing protocols are modified and processing parameters optimized. It is essential to improve the organoleptic properties of camel-milk feta cheese. Future research should consider the use of natural additives such as spices or condiments to improve flavour, aroma, texture, antioxidant and antimicrobial properties, and shelf life of the cheese.
Aim:
The study aimed to develop feta-type cheese from camel milk and evaluate its physicochemical properties and sensory acceptability.
Methods:
Milk samples were obtained from dromedary camels (Camelus dromedarius) kept at the Tsabong Ecotourism Camel Park in Botswana. Feta-type cheese was developed using WhiteDaily 41 culture, which contains mesophilic and thermophilic lactic acid bacteria, and camel chymosin (CHY-MAX M1000). Standard procedures were used to assess physicochemical characteristics and sensory-based consumer acceptability. Cow-milk feta cheese produced using the same procedure served as the control. Mann–Whitney test was used to compare quality parameters of the camel- and cow-milk cheeses.
Results:
The results showed that producing feta-type cheese from camel milk was more difficult than from cow milk, and the yield from camel milk was slightly lower. Except for ash and fat content, no significant differences (p > 0.05) were found between the two cheese types. Cow-milk feta had significantly higher ash and fat levels (p < 0.05) than camel-milk feta. Overall, camel-milk feta displayed physicochemical characteristics comparable to those of cow-milk feta. The sensory acceptability test revealed that aroma, texture, taste, and overall acceptability scores were significantly higher (p < 0.05) for cow-milk feta than for camel-milk feta. However, colour did not differ significantly (p > 0.05) between the two cheeses.
Conclusions:
The findings show that making feta-type cheese from camel milk is possible, provided that manufacturing protocols are modified and processing parameters optimized. It is essential to improve the organoleptic properties of camel-milk feta cheese. Future research should consider the use of natural additives such as spices or condiments to improve flavour, aroma, texture, antioxidant and antimicrobial properties, and shelf life of the cheese.
DOI: https://doi.org/10.37349/eff.2026.1010135
Aim:
Dysfunctional breathing (DB) is a common comorbidity in asthma, yet its objective characterisation remains challenging due to reliance on subjective questionnaires. This study aimed to determine whether quantifiable breathing pattern parameters can be used to characterise asthma patients with perceived DB from those without DB.
Methods:
This observational cross-sectional study involved 122 adults with physician-diagnosed asthma (GINA Steps 2–5). Participants completed the Nijmegen Questionnaire (NQ) to determine DB (NQ > 23) or non-DB (NDB). Resting breathing was recorded for 5 minutes using structured light plethysmography (SLP), a contactless optical motion-analysis system that quantifies thoracoabdominal displacement. Extracted parameters included respiratory rate (RR), inspiration time (Ti), expiration time (Te), Ti/total breath cycle duration (Ttot), and the ratio of ribcage to abdominal displacement during the inspiration phase (RCampinsp/ABampinsp). Both absolute values and within-subject variability [coefficient of variation expressed in percentage (CoV%)] were estimated. Between-group comparisons used Mann-Whitney U tests. Two binary logistic regression models evaluated the predictive value of mean parameters and their variability for characterising DB.
Results:
Of the 122 participants, 38 asthmatic patients were determined with DB. The DB group showed significantly higher RR and lower Ti and Te, but no differences in Ti/Ttot or RCampinsp/ABampinsp. In contrast, within-subject variability across all parameters was significantly greater in the DB group. The regression model using absolute values showed limited predictive power (R2 = 0.251). The model incorporating variability demonstrated substantially improved predictive power (R2 = 0.540), with CoV% RR, Te, Ti/Ttot, and RCampinsp/ABampinsp emerging as significant predictors.
Conclusions:
Asthma patients with DB exhibit breathing-pattern alterations, most notably increased within-subject variability of timing and TA movement parameters. Breathing pattern variability may be a promising surrogate marker to characterise DB, highlighting the value of dynamic objective physiological assessment of breathing beyond conventional symptom-based assessments of DB.
Aim:
Dysfunctional breathing (DB) is a common comorbidity in asthma, yet its objective characterisation remains challenging due to reliance on subjective questionnaires. This study aimed to determine whether quantifiable breathing pattern parameters can be used to characterise asthma patients with perceived DB from those without DB.
Methods:
This observational cross-sectional study involved 122 adults with physician-diagnosed asthma (GINA Steps 2–5). Participants completed the Nijmegen Questionnaire (NQ) to determine DB (NQ > 23) or non-DB (NDB). Resting breathing was recorded for 5 minutes using structured light plethysmography (SLP), a contactless optical motion-analysis system that quantifies thoracoabdominal displacement. Extracted parameters included respiratory rate (RR), inspiration time (Ti), expiration time (Te), Ti/total breath cycle duration (Ttot), and the ratio of ribcage to abdominal displacement during the inspiration phase (RCampinsp/ABampinsp). Both absolute values and within-subject variability [coefficient of variation expressed in percentage (CoV%)] were estimated. Between-group comparisons used Mann-Whitney U tests. Two binary logistic regression models evaluated the predictive value of mean parameters and their variability for characterising DB.
Results:
Of the 122 participants, 38 asthmatic patients were determined with DB. The DB group showed significantly higher RR and lower Ti and Te, but no differences in Ti/Ttot or RCampinsp/ABampinsp. In contrast, within-subject variability across all parameters was significantly greater in the DB group. The regression model using absolute values showed limited predictive power (R2 = 0.251). The model incorporating variability demonstrated substantially improved predictive power (R2 = 0.540), with CoV% RR, Te, Ti/Ttot, and RCampinsp/ABampinsp emerging as significant predictors.
Conclusions:
Asthma patients with DB exhibit breathing-pattern alterations, most notably increased within-subject variability of timing and TA movement parameters. Breathing pattern variability may be a promising surrogate marker to characterise DB, highlighting the value of dynamic objective physiological assessment of breathing beyond conventional symptom-based assessments of DB.
DOI: https://doi.org/10.37349/eaa.2026.1009122
Aim:
This study aimed to evaluate the real-world efficacy and safety of lorlatinib in patients with anaplastic lymphoma kinase (ALK)-rearranged metastatic non-small cell lung cancer (NSCLC) after the failure of at least one prior ALK tyrosine kinase inhibitor (TKI).
Methods:
The dataset included 82 subjects with metastatic NSCLC, who received lorlatinib upon compassionate use program or routine treatment between January 2017 and May 2025. All patients involved in this study responded to a prior ALK inhibitor for at least 4 months and switched to the above drug due to disease progression.
Results:
The overall objective response rate (ORR) was 64.6%, with the disease control rate (DCR) of 96.3%. Among 65 patients with brain metastases, the intracranial ORR and DCR were 66.2% and 96.9%, respectively. After a median follow-up of 82.7 months, the median progression-free survival (PFS) was 66.7 months (95% CI, 40.5–75.0 months), while the median overall survival (OS) was not reached (NR) (95% CI, NR–NR). Patients who had benefited from prior ALK TKI for more than 12 months achieved significantly longer PFS (NR vs. 34.0 months; p = 0.013) and OS (NR vs. 39.4 months; p = 0.002). Multivariate analysis showed that prior response to ALK TKI of less than 12 months was an independent negative predictor of survival (PFS: p = 0.039, OS: p = 0.027). Treatment-related adverse events (AEs) were reported in 75.6% of patients, with 8.1% experiencing grade 3 or higher toxicity; no treatment-related AEs led to permanent discontinuation of lorlatinib.
Conclusions:
This real-world dataset demonstrates an unusually pronounced benefit from lorlatinib in selected patients who progressed on early-generation TKIs, especially in long-term responders to prior therapy. However, the observed outcomes should be interpreted within the context of patient selection. The enrichment for prior responders limits the generalizability to unselected post-TKI populations, including those with primary resistance.
Aim:
This study aimed to evaluate the real-world efficacy and safety of lorlatinib in patients with anaplastic lymphoma kinase (ALK)-rearranged metastatic non-small cell lung cancer (NSCLC) after the failure of at least one prior ALK tyrosine kinase inhibitor (TKI).
Methods:
The dataset included 82 subjects with metastatic NSCLC, who received lorlatinib upon compassionate use program or routine treatment between January 2017 and May 2025. All patients involved in this study responded to a prior ALK inhibitor for at least 4 months and switched to the above drug due to disease progression.
Results:
The overall objective response rate (ORR) was 64.6%, with the disease control rate (DCR) of 96.3%. Among 65 patients with brain metastases, the intracranial ORR and DCR were 66.2% and 96.9%, respectively. After a median follow-up of 82.7 months, the median progression-free survival (PFS) was 66.7 months (95% CI, 40.5–75.0 months), while the median overall survival (OS) was not reached (NR) (95% CI, NR–NR). Patients who had benefited from prior ALK TKI for more than 12 months achieved significantly longer PFS (NR vs. 34.0 months; p = 0.013) and OS (NR vs. 39.4 months; p = 0.002). Multivariate analysis showed that prior response to ALK TKI of less than 12 months was an independent negative predictor of survival (PFS: p = 0.039, OS: p = 0.027). Treatment-related adverse events (AEs) were reported in 75.6% of patients, with 8.1% experiencing grade 3 or higher toxicity; no treatment-related AEs led to permanent discontinuation of lorlatinib.
Conclusions:
This real-world dataset demonstrates an unusually pronounced benefit from lorlatinib in selected patients who progressed on early-generation TKIs, especially in long-term responders to prior therapy. However, the observed outcomes should be interpreted within the context of patient selection. The enrichment for prior responders limits the generalizability to unselected post-TKI populations, including those with primary resistance.
DOI: https://doi.org/10.37349/etat.2026.1002366
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a debilitating condition of the urogenital system, with an elusive and multifactorial pathogenesis. Recent data show that there is a potential interplay between dysregulated autophagy and altered exosomal communication that may contribute to the persistent inflammation and pain characteristic of CP/CPPS. This review synthesizes recent advances to propose a hypothetical model: cellular stress in the prostate may trigger dysfunctional autophagy, which could reprogram secreted exosomes biogenesis and cargo in a series of lipid-raft microdomain-involved mechanisms and secretory autophagy. The outcomes of this process include the release of pro-inflammatory cytokines (e.g., IL-1β, TNF-α) enriched exosomes, damage-associated molecular patterns (DAMPs), microRNAs (e.g., miR-155), and fibrotic mediators (e.g., TGF-β1). These signalosomes are hypothesized to transmit the inflammatory and nociceptive signals and may contribute to coordinating the dysregulation of immune cells (such as the M1 polarization of macrophages), sensitization of neurons, and tissue fibrosis, thereby potentially perpetuating the presence of a chronic disease. We critically assess the available evidence based on human studies, animal models, and in vitro systems, but recognize that there is a present requirement for additional CP/CPPS-specific mechanistic evidence. Furthermore, we explore the translational implications of this axis, discussing its promise for yielding novel exosome-based diagnostic biomarkers and its potential as a therapeutic target, while also highlighting the significant preclinical challenges and risks that must be overcome. Ultimately, the autophagy-exosome axis presents a new, integrative concept of CP/CPPS, which shifts the paradigm to the mechanisms of intercellular communication and provides new possibilities to carry out mechanism-selective research and future treatment options.
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a debilitating condition of the urogenital system, with an elusive and multifactorial pathogenesis. Recent data show that there is a potential interplay between dysregulated autophagy and altered exosomal communication that may contribute to the persistent inflammation and pain characteristic of CP/CPPS. This review synthesizes recent advances to propose a hypothetical model: cellular stress in the prostate may trigger dysfunctional autophagy, which could reprogram secreted exosomes biogenesis and cargo in a series of lipid-raft microdomain-involved mechanisms and secretory autophagy. The outcomes of this process include the release of pro-inflammatory cytokines (e.g., IL-1β, TNF-α) enriched exosomes, damage-associated molecular patterns (DAMPs), microRNAs (e.g., miR-155), and fibrotic mediators (e.g., TGF-β1). These signalosomes are hypothesized to transmit the inflammatory and nociceptive signals and may contribute to coordinating the dysregulation of immune cells (such as the M1 polarization of macrophages), sensitization of neurons, and tissue fibrosis, thereby potentially perpetuating the presence of a chronic disease. We critically assess the available evidence based on human studies, animal models, and in vitro systems, but recognize that there is a present requirement for additional CP/CPPS-specific mechanistic evidence. Furthermore, we explore the translational implications of this axis, discussing its promise for yielding novel exosome-based diagnostic biomarkers and its potential as a therapeutic target, while also highlighting the significant preclinical challenges and risks that must be overcome. Ultimately, the autophagy-exosome axis presents a new, integrative concept of CP/CPPS, which shifts the paradigm to the mechanisms of intercellular communication and provides new possibilities to carry out mechanism-selective research and future treatment options.
DOI: https://doi.org/10.37349/ei.2026.1003247
Aim:
Chitosan (CHS)-based nanoparticulate systems have gained much interest due to their high drug loading capacity and the simplicity of their fabrication. The physical properties of two types of curcumin-loaded CHS nanoparticles (CHS-NPs) were determined and compared. A new in-vitro release method was developed based on mathematical modeling in which the drug is first released from the NP into the surrounding medium and subsequently diffuses through the membrane.
Methods:
Curcumin-loaded CHS-NPs were fabricated by ionotropic gelation using sodium tripolyphosphate (TPP) and sodium hexametaphosphate (SHMP) crosslinking, and characterized by NP tracking analysis, loading capacity, zeta potential, Fourier transform infrared spectroscopy (FTIR), and in-vitro release rates.
Results:
The data showed that compared to SHMP crosslinked CHS-NPs, TPP crosslinking demonstrated a decrease in entrapment efficiency at a relatively high concentration of the agent, probably by narrowing the space between the polymeric chains. As indicated by zeta potential measurements, TPP crosslinking at all levels was more uniformly distributed inside the NPs, whereas the higher molecular weight SHMP at a low concentration creates NPs mostly by binding onto the surface. It was found that the release rates of curcumin from CHS-NPs crosslinked by SHMP at higher concentrations were about twice as high as the release rates of curcumin from TPP-crosslinked CHS-NPs, accompanied by notable lag times.
Conclusions:
This significant increase in the release rates of curcumin from SHMP-crosslinked CHS-NPs is explained by the large spatial structure of this crosslinker compared to the small TPP molecules. This study advances the literature on drug diffusion by making it possible to accurately determine its release from nanoparticulate systems.
Aim:
Chitosan (CHS)-based nanoparticulate systems have gained much interest due to their high drug loading capacity and the simplicity of their fabrication. The physical properties of two types of curcumin-loaded CHS nanoparticles (CHS-NPs) were determined and compared. A new in-vitro release method was developed based on mathematical modeling in which the drug is first released from the NP into the surrounding medium and subsequently diffuses through the membrane.
Methods:
Curcumin-loaded CHS-NPs were fabricated by ionotropic gelation using sodium tripolyphosphate (TPP) and sodium hexametaphosphate (SHMP) crosslinking, and characterized by NP tracking analysis, loading capacity, zeta potential, Fourier transform infrared spectroscopy (FTIR), and in-vitro release rates.
Results:
The data showed that compared to SHMP crosslinked CHS-NPs, TPP crosslinking demonstrated a decrease in entrapment efficiency at a relatively high concentration of the agent, probably by narrowing the space between the polymeric chains. As indicated by zeta potential measurements, TPP crosslinking at all levels was more uniformly distributed inside the NPs, whereas the higher molecular weight SHMP at a low concentration creates NPs mostly by binding onto the surface. It was found that the release rates of curcumin from CHS-NPs crosslinked by SHMP at higher concentrations were about twice as high as the release rates of curcumin from TPP-crosslinked CHS-NPs, accompanied by notable lag times.
Conclusions:
This significant increase in the release rates of curcumin from SHMP-crosslinked CHS-NPs is explained by the large spatial structure of this crosslinker compared to the small TPP molecules. This study advances the literature on drug diffusion by making it possible to accurately determine its release from nanoparticulate systems.
DOI: https://doi.org/10.37349/eds.2026.1008157
Aim:
To explore preliminary signals of change associated with a digitalized educational innovation—The Vital House (La Casa Vital)—on psychological flexibility and introspection among prospective secondary-school teachers in Spain, with the broader goal of promoting mental health competencies relevant to adolescent well-being.
Methods:
A total of 82 students enrolled in a Master’s program in teacher training at a Spanish public university participated in a 10-session intervention over 2.5 months (approximately 20 hours total). The Vital House model, a metaphorical representation of personal identity through “rooms” symbolizing life roles, was adapted into a digital format. Each room included interactive resources designed to address key psychosocial variables, including self‑efficacy, emotional regulation, and cognitive defusion. Participants reflected on their learning histories and the influence of significant figures, including teachers, on adult identity. Pre- and post-intervention measures assessed components of the ACT Hexaflex model (ad-hoc questionnaire) and introspective capacity (Self-Reflection and Insight Scale-Short Form).
Results:
Paired-sample analyses indicated pre–post differences on five of six ACT processes: values (p = 0.048), mindfulness (p = 0.014), self-as-context (p < 0.001), cognitive defusion (p = 0.034), acceptance (p = 0.019), and on introspective capacity (p = 0.008). Effect sizes were in the small‑to‑moderate range, with Cohen’s d values ranging from 0.22 (small) to 0.42 (moderate). These findings should be interpreted cautiously given the design.
Conclusions:
In this pilot‑level, single‑group study, Vital House showed preliminary indications of promise for enhancing psychological flexibility and introspection in teacher training. However, the absence of a control/comparison group, the potential influence of concurrent course content, maturation, historical events, and repeated‑testing effects, as well as the lack of post‑intervention follow‑up, limit causal inference and claims about durability. Future controlled studies with follow‑up are warranted to evaluate efficacy, mechanisms, and maintenance, and to assess scalability across educational contexts.
Aim:
To explore preliminary signals of change associated with a digitalized educational innovation—The Vital House (La Casa Vital)—on psychological flexibility and introspection among prospective secondary-school teachers in Spain, with the broader goal of promoting mental health competencies relevant to adolescent well-being.
Methods:
A total of 82 students enrolled in a Master’s program in teacher training at a Spanish public university participated in a 10-session intervention over 2.5 months (approximately 20 hours total). The Vital House model, a metaphorical representation of personal identity through “rooms” symbolizing life roles, was adapted into a digital format. Each room included interactive resources designed to address key psychosocial variables, including self‑efficacy, emotional regulation, and cognitive defusion. Participants reflected on their learning histories and the influence of significant figures, including teachers, on adult identity. Pre- and post-intervention measures assessed components of the ACT Hexaflex model (ad-hoc questionnaire) and introspective capacity (Self-Reflection and Insight Scale-Short Form).
Results:
Paired-sample analyses indicated pre–post differences on five of six ACT processes: values (p = 0.048), mindfulness (p = 0.014), self-as-context (p < 0.001), cognitive defusion (p = 0.034), acceptance (p = 0.019), and on introspective capacity (p = 0.008). Effect sizes were in the small‑to‑moderate range, with Cohen’s d values ranging from 0.22 (small) to 0.42 (moderate). These findings should be interpreted cautiously given the design.
Conclusions:
In this pilot‑level, single‑group study, Vital House showed preliminary indications of promise for enhancing psychological flexibility and introspection in teacher training. However, the absence of a control/comparison group, the potential influence of concurrent course content, maturation, historical events, and repeated‑testing effects, as well as the lack of post‑intervention follow‑up, limit causal inference and claims about durability. Future controlled studies with follow‑up are warranted to evaluate efficacy, mechanisms, and maintenance, and to assess scalability across educational contexts.
DOI: https://doi.org/10.37349/edht.2026.101191
This article belongs to the special issue Digital Health Innovations in the Battle Against Psychological Problems: Progress, Hurdles, and Prospects
Aim:
This study aimed to evaluate the effects of essential oil nanoemulsion-enriched diets on feed acceptability, growth performance, proximate composition, and digestive gland histology of farmed Cornu aspersum maximum.
Methods:
A total of 2,000 juvenile snails were divided into four dietary treatments for a two-month feeding experiment. The control group received a commercial poultry feed, while the experimental groups were fed the same diet supplemented with an essential oil nanoemulsion at concentrations of 1 mL/kg (T1), 3 mL/kg (T2), and 5 mL/kg (T3). Eight samplings were conducted to measure snail diameter, weight, mortality, and feed residues. At the end of the experiment, fillet proximate composition and histopathological alterations of the digestive gland tissue were evaluated.
Results:
A tendency toward increased snail weight was observed across all treatments. Diet enrichment led to significantly higher fillet protein content across all treatment groups (T1, T2, and T3) compared to the control, while lipid content was highest in T1. Histopathological examination revealed enlargement of hepatic ducts in T1, apoptosis of digestive cells in T2, and necrosis of digestive and calcium cells along with thinned epithelium lining in T3.
Conclusions:
Dietary supplementation with essential oil nanoemulsion did not negatively affect snail growth and resulted in heavier snails with increased fillet protein content. However, histopathological evidence of toxicity rendered higher supplementation levels (T2 and T3) unsuitable. Enrichment at 1 mL/kg appears to be suitable for use in commercial snail farming.
Aim:
This study aimed to evaluate the effects of essential oil nanoemulsion-enriched diets on feed acceptability, growth performance, proximate composition, and digestive gland histology of farmed Cornu aspersum maximum.
Methods:
A total of 2,000 juvenile snails were divided into four dietary treatments for a two-month feeding experiment. The control group received a commercial poultry feed, while the experimental groups were fed the same diet supplemented with an essential oil nanoemulsion at concentrations of 1 mL/kg (T1), 3 mL/kg (T2), and 5 mL/kg (T3). Eight samplings were conducted to measure snail diameter, weight, mortality, and feed residues. At the end of the experiment, fillet proximate composition and histopathological alterations of the digestive gland tissue were evaluated.
Results:
A tendency toward increased snail weight was observed across all treatments. Diet enrichment led to significantly higher fillet protein content across all treatment groups (T1, T2, and T3) compared to the control, while lipid content was highest in T1. Histopathological examination revealed enlargement of hepatic ducts in T1, apoptosis of digestive cells in T2, and necrosis of digestive and calcium cells along with thinned epithelium lining in T3.
Conclusions:
Dietary supplementation with essential oil nanoemulsion did not negatively affect snail growth and resulted in heavier snails with increased fillet protein content. However, histopathological evidence of toxicity rendered higher supplementation levels (T2 and T3) unsuitable. Enrichment at 1 mL/kg appears to be suitable for use in commercial snail farming.
DOI: https://doi.org/10.37349/eff.2026.1010134
Circadian rhythms are intrinsic 24-hour cycles that coordinate key metabolic processes, including glucose homeostasis, lipid metabolism, and energy expenditure. Disruption of these rhythms, due to sleep disturbances, shift work, or irregular feeding schedules, contributes to the development of obesity, insulin resistance, and dyslipidemia. Core clock genes, including circadian locomotor output cycles kaput (CLOCK), brain and muscle ARNT-like 1 (BMAL1), period gene (PER), and cryptochrome (CRY), play a central role in orchestrating these metabolic pathways. Chronotherapy, aligning lifestyle, behavioral, and pharmacologic interventions with circadian timing, represents a promising, yet underexplored, strategy for metabolic disease management. Evidence suggests that interventions such as time-restricted feeding, light therapy, pharmacologic modulators of clock gene expression, and wearable technology can improve glucose control, lipid profiles, and body weight. This review synthesizes current knowledge on the molecular regulation of metabolism by circadian clocks, elucidates mechanistic links between rhythm disruption and metabolic dysfunction, and explores translational strategies to restore circadian homeostasis. By targeting circadian rhythms, personalized and cost-effective interventions can be developed to mitigate the global burden of metabolic disorders. Future research should focus on large-scale clinical trials, precision chronotherapy, and integration of wearable devices to optimize the timing of interventions, ultimately enhancing treatment efficacy and long-term metabolic health.
Circadian rhythms are intrinsic 24-hour cycles that coordinate key metabolic processes, including glucose homeostasis, lipid metabolism, and energy expenditure. Disruption of these rhythms, due to sleep disturbances, shift work, or irregular feeding schedules, contributes to the development of obesity, insulin resistance, and dyslipidemia. Core clock genes, including circadian locomotor output cycles kaput (CLOCK), brain and muscle ARNT-like 1 (BMAL1), period gene (PER), and cryptochrome (CRY), play a central role in orchestrating these metabolic pathways. Chronotherapy, aligning lifestyle, behavioral, and pharmacologic interventions with circadian timing, represents a promising, yet underexplored, strategy for metabolic disease management. Evidence suggests that interventions such as time-restricted feeding, light therapy, pharmacologic modulators of clock gene expression, and wearable technology can improve glucose control, lipid profiles, and body weight. This review synthesizes current knowledge on the molecular regulation of metabolism by circadian clocks, elucidates mechanistic links between rhythm disruption and metabolic dysfunction, and explores translational strategies to restore circadian homeostasis. By targeting circadian rhythms, personalized and cost-effective interventions can be developed to mitigate the global burden of metabolic disorders. Future research should focus on large-scale clinical trials, precision chronotherapy, and integration of wearable devices to optimize the timing of interventions, ultimately enhancing treatment efficacy and long-term metabolic health.
DOI: https://doi.org/10.37349/eemd.2026.101467
Background:
Multiple sclerosis (MS) is a chronic, autoimmune, inflammatory disease that affects the central nervous system. Although the true etiology of MS remains unknown, recent research suggests that it arises from a combination of genetic vulnerability and environmental factors. The human leukocyte antigen (HLA) region is a highly polymorphic locus on chromosome 6 encoding antigen-presenting molecules central to adaptive immunity. MS exhibits significant genetic and geographic heterogeneity, reflecting complex interactions between HLA polymorphisms and environmental influences. Risk and protective alleles differ across populations, reinforcing the importance of studying such variations to better understand the disease’s pathogenesis and guide therapeutic strategies.
Methods:
This systematic review followed the “Preferred Reporting Items for Systematic reviews and Meta-Analyses” (PRISMA) guidelines, and a bibliographic search was conducted in the Medline (PubMed) and Web of Science databases using the keywords “Multiple Sclerosis”, “Genetic Polymorphisms”, “SNPs”, and “Human Leukocyte Antigen”.
Results:
Twenty-one studies were included, comprising a total of over 50,000 participants across diverse populations. The reviewed studies demonstrate that the alleles DRB1*15:01, DQB1*06:02, DRB1*03:01, DRB1*04:01, DRB1*15:03, DPB1*03:01, as well as the haplotypes DRB1*15:01~DQB1*06:02 and DRB1*15:01~DQA1*01:02~DQB1*06:02, show high expression and are strongly associated with MS susceptibility. In contrast, the alleles A*02:01 and DRB1*01:01 have shown a protective role.
Discussion:
The evidence confirms a central role of HLA class II alleles and conserved extended haplotypes, particularly DRB1*15:01-containing haplotypes, in MS susceptibility, while highlighting protective alleles and marked variability across ancestral backgrounds. These findings underscore the importance of high-resolution HLA typing, standardized haplotype definitions and inclusion of diverse populations to refine MS risk estimates.
Background:
Multiple sclerosis (MS) is a chronic, autoimmune, inflammatory disease that affects the central nervous system. Although the true etiology of MS remains unknown, recent research suggests that it arises from a combination of genetic vulnerability and environmental factors. The human leukocyte antigen (HLA) region is a highly polymorphic locus on chromosome 6 encoding antigen-presenting molecules central to adaptive immunity. MS exhibits significant genetic and geographic heterogeneity, reflecting complex interactions between HLA polymorphisms and environmental influences. Risk and protective alleles differ across populations, reinforcing the importance of studying such variations to better understand the disease’s pathogenesis and guide therapeutic strategies.
Methods:
This systematic review followed the “Preferred Reporting Items for Systematic reviews and Meta-Analyses” (PRISMA) guidelines, and a bibliographic search was conducted in the Medline (PubMed) and Web of Science databases using the keywords “Multiple Sclerosis”, “Genetic Polymorphisms”, “SNPs”, and “Human Leukocyte Antigen”.
Results:
Twenty-one studies were included, comprising a total of over 50,000 participants across diverse populations. The reviewed studies demonstrate that the alleles DRB1*15:01, DQB1*06:02, DRB1*03:01, DRB1*04:01, DRB1*15:03, DPB1*03:01, as well as the haplotypes DRB1*15:01~DQB1*06:02 and DRB1*15:01~DQA1*01:02~DQB1*06:02, show high expression and are strongly associated with MS susceptibility. In contrast, the alleles A*02:01 and DRB1*01:01 have shown a protective role.
Discussion:
The evidence confirms a central role of HLA class II alleles and conserved extended haplotypes, particularly DRB1*15:01-containing haplotypes, in MS susceptibility, while highlighting protective alleles and marked variability across ancestral backgrounds. These findings underscore the importance of high-resolution HLA typing, standardized haplotype definitions and inclusion of diverse populations to refine MS risk estimates.
DOI: https://doi.org/10.37349/ent.2026.1004147
There is a growing appreciation of the role of mitochondria in determining the interactions of CNS astrocytes, microglia, and neurons. The influence of circadian and systemic processes in regulating these interactions is relatively underexplored. Recent work has indicated the importance of night-time dampening and resetting in the pathoetiology of a diverse array of aging-associated medical conditions, including neurodegenerative disorders. The 10-fold decrease in pineal melatonin at night between childhood and the 9th decade of life is a major determinant of how aging associates with neurodegenerative disorders, cardiovascular disorders, and a wide range of tumors. It is proposed that the beneficial effects of pineal melatonin are mediated via its upregulation of the mitochondria-derived peptides (MDPs), including humanin. Although potentially induced in all mitochondria-containing cells, humanin is primarily produced in the CNS by astrocytes. The capacity of pineal melatonin to increase astrocyte humanin leads to the induction of the local melatonergic pathway in microglia to shift microglia from a pro-inflammatory M1-like to prophagocytic M2-like phenotype. In neurons, astrocyte-derived humanin optimizes mitochondrial function and decreases oxidant production to increase function and survival, possibly also involving mitochondrial melatonergic pathway upregulation. Concurrent effects of pineal melatonin in decreasing gut dysbiosis/permeability and stimulating oxytocin to activate the vagal nerve contribute to more optimized dampening and resetting that influences CNS interactions of glia and neurons. Overall, the conceptualizations of how astrocyte, microglial, and neuronal mitochondria interact require integration with wider circadian and systemic processes. A plethora of novel research implications are highlighted.
There is a growing appreciation of the role of mitochondria in determining the interactions of CNS astrocytes, microglia, and neurons. The influence of circadian and systemic processes in regulating these interactions is relatively underexplored. Recent work has indicated the importance of night-time dampening and resetting in the pathoetiology of a diverse array of aging-associated medical conditions, including neurodegenerative disorders. The 10-fold decrease in pineal melatonin at night between childhood and the 9th decade of life is a major determinant of how aging associates with neurodegenerative disorders, cardiovascular disorders, and a wide range of tumors. It is proposed that the beneficial effects of pineal melatonin are mediated via its upregulation of the mitochondria-derived peptides (MDPs), including humanin. Although potentially induced in all mitochondria-containing cells, humanin is primarily produced in the CNS by astrocytes. The capacity of pineal melatonin to increase astrocyte humanin leads to the induction of the local melatonergic pathway in microglia to shift microglia from a pro-inflammatory M1-like to prophagocytic M2-like phenotype. In neurons, astrocyte-derived humanin optimizes mitochondrial function and decreases oxidant production to increase function and survival, possibly also involving mitochondrial melatonergic pathway upregulation. Concurrent effects of pineal melatonin in decreasing gut dysbiosis/permeability and stimulating oxytocin to activate the vagal nerve contribute to more optimized dampening and resetting that influences CNS interactions of glia and neurons. Overall, the conceptualizations of how astrocyte, microglial, and neuronal mitochondria interact require integration with wider circadian and systemic processes. A plethora of novel research implications are highlighted.
DOI: https://doi.org/10.37349/en.2026.1006132
