Retinal artery occlusion (RAO) is an emergency condition causing acute retinal ischemia and is considered an equivalent of ischemic stroke. The occurrence of an episode of RAO is associated with significant impairment of visual functions and correlates with an increased risk of future vascular events. Although RAO requires immediate diagnosis and treatment, there are currently no clear guidelines specifying optimal management. This review discusses current and future therapeutic strategies following an episode of RAO, including secondary prevention.

Regular training imposes repeated physiological demands that activate neuroendocrine stress regulation, with the hypothalamic–pituitary–adrenal (HPA) axis playing a central role. Cortisol supports metabolic regulation and adaptation to exercise-related stress; however, prolonged exposure to high training loads combined with insufficient recovery may lead to functional alterations in HPA axis regulation, potentially affecting exercise capacity and recovery processes. This narrative review synthesizes current evidence on HPA axis dysregulation in regularly training individuals, with particular emphasis on its relevance for exercise capacity and recovery. The review includes peer-reviewed experimental, observational, longitudinal, and sport-specific studies addressing HPA axis physiology, cortisol secretion dynamics, cortisol awakening response (CAR), training load, fatigue, overreaching, overtraining, exercise capacity, and recovery in physically active populations. Available evidence indicates that cumulative training stress is associated with changes in basal cortisol secretion, diurnal cortisol rhythm, and CAR. Functional alterations in HPA axis activity may influence metabolic efficiency, neuromuscular function, stress responsiveness, and performance stability. These responses appear to occur along an adaptive–maladaptive continuum and are strongly modulated by individual characteristics, training structure, and recovery adequacy. Importantly, many training-related disturbances of HPA axis function seem to be time-dependent and at least partially reversible. Viewing HPA axis dysregulation as a dynamic and functional process may improve interpretation of training responses, while longitudinal assessment of cortisol-related markers, interpreted within the broader training and recovery context, may provide valuable insight into individual stress adaptability in regularly training individuals.

Background Crohn’s disease (CD) is a chronic inflammatory bowel disease commonly diagnosed in women of reproductive age. While treatments have improved over the years, pregnancy in women with CD still presents certain challenges. Recent findings suggest a strong link between disease activity and pregnancy outcomes. Aim To summarize contemporary evidence on pregnancy in women with CD, focusing on pathophysiological and clinical considerations, maternal outcomes, fetal and neonatal outcomes, disease monitoring during pregnancy, and selected high-risk clinical scenarios. Material and Methods This narrative review included articles published between 2015 and 2025 on pregnancy outcomes in women with CD. Relevant publications were identified using keywords such as CD, IBD, pregnancy, maternal and neonatal outcomes, disease activity, and monitoring. The analysis drew on clinical guidelines, observational studies, and narrative reviews, with no formal systematic review or meta-analysis applied. Results Disease activity at conception and during pregnancy emerged as the strongest determinant of pregnancy outcomes. Active disease was linked to higher risks of exacerbation, preterm birth (PTB), impaired fetal growth, and complications. Pregnancies conceived in remission were more often stable, with outcomes resembling those of the general population. Improvements over time reflect better disease monitoring, therapy, and multidisciplinary management. Conclusions Pregnancy outcomes in women with CD are primarily influenced by disease activity, not the diagnosis itself. Preconception counseling, remission, and structured monitoring are essential for optimizing maternal and fetal outcomes.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized byprogressive motor neuron loss and marked biological heterogeneity. Advances in moleculargenetics and biomarker research have redefined ALS as a spectrum of molecularly distinctsubtypes, creating new opportunities for disease-modifying therapeutic development.Aim To synthesize contemporary evidence on disease-modifying therapies in ALS, with a focus onclinical trial outcomes, validated biomarkers, and molecular targets that inform precisionmedicine approaches.Material and Methods This narrative review integrates peer-reviewed original studies, clinical trials, and highqualityreview articles published predominantly between 2017 and 2025. Literature wasselected based on relevance to ALS molecular pathophysiology, targeted therapeuticstrategies, biomarker development, and clinical trial methodology. Data were synthesizedqualitatively, emphasizing target engagement, biomarker modulation, and translationallimitations.Results ALS pathogenesis converges on shared downstream mechanisms, including RNAdysmetabolism, impaired proteostasis, mitochondrial dysfunction, and neuroinflammation,despite diverse genetic drivers. Antisense oligonucleotide (ASO) therapies - particularlytargeting SOD1 - have demonstrated robust biological efficacy, including molecular targetengagement and neurofilament light chain (NfL) modulation. NfL has emerged as the mostrobustly validated biomarker for prognosis, patient stratification, and pharmacodynamicassessment, although its predictive value for long-term clinical benefit remains underevaluation. Non–ASO disease-modifying approaches have shown variable clinical outcomes,highlighting methodological and biological challenges. ConclusionsDisease-modifying intervention in ALS is biologically feasible but remains limited by delayeddiagnosis, disease heterogeneity, and conventional trial design constraints.

Background: Thyroid dysfunction is one of the most common endocrine disorders and represents an important public health issue. Its etiology is multifactorial and includes genetic, immunological, environmental, and dietary factors. A vegetarian diet, rich in plant-based foods, provides bioactive compounds with antioxidant and anti-inflammatory properties that may influence immune regulation. However, poorly balanced vegetarian diets may result in deficiencies of nutrients essential for thyroid function, including iodine, selenium, and vitamin B12.Aim: This study aims to review current scientific evidence on the effects of a vegetarian diet on thyroid function, focusing on potential benefits, risks, and the role of supplementation.Materials and methods: A narrative literature review was conducted using publications from PubMed, Scopus, and Web of Science databases published between 2010 and 2025. Articles addressing vegetarian diets, thyroid function, autoimmune thyroid diseases, and micronutrient supplementation were analyzed.Results: Evidence suggests that a vegetarian diet may have both beneficial and adverse effects on thyroid health. Benefits include higher intake of antioxidants, lower body weight, and a potentially reduced risk of hyperthyroidism. Conversely, vegetarians show a higher risk of deficiencies in iodine, selenium, vitamin B12, and omega-3 fatty acids, which may contribute to hypothyroidism and exacerbate autoimmune thyroid diseases. Regular monitoring and targeted supplementation are therefore recommended.Conclusions: A well-planned vegetarian diet can support thyroid health when appropriate supplementation is ensured. Increased awareness of potential nutrient deficiencies, particularly in individuals with thyroid disorders and in pregnant women, is essential. Further research is needed to establish optimal dietary strategies for thyroid health in vegetarian populations.