ABSTRACT
Aim: The aim of this study is to determine the dynamics of histoarchitectural changes in the bone-ceramic regenerate after transplantation β-tricalcium phosphate into an experimental defect in the rabbit mandible.
Materials and Methods: Adult male rabbits aged 6-7 months and weighing 2.5-3 kg were used for the study. The control group consisted of animals with a bone defect that healed under a blood clot. The experimental group consisted of rabbits in which the bone defect was filled with β-tricalcium phosphate.
Post-traumatic monitoring was conducted over 84 days using scanning electron microscopy and morphometric analysis of three parameters of the regenerate.
Results: Studying the surface relief characteristics of the experimental bone defect in the lower jaw after implantation of the β-tricalcium phosphate material revealed numerous regenerative changes that occurred after the injury and correlated with the dynamics of changes in the relative volume of bone tissue, osteoplastic material, and connective tissue in the regenerate. Morphometric analysis of the regenerate showed a phased character of the dynamics of changes.
Conclusions: The study found that the relative volume of bone tissue in the regenerate increased over time, and at the end of the experiment, it was statistically similar to the control group.
KEY WORDS: bone regeneration, mandible/lower jaw, β-tricalcium phosphate morphometry, scanning electron microscopy (SEM)

УДК: 616-056.3:616.24]-06:616.24-002]-07:616.155.321-07]-092.9

Актуальність. Проблема захворювань бронхолегеневого апарату залишається актуаль-ною для сьогодення. На думку фахівців, одним із провідних впливів на розвиток та прояви легеневої патології вважається стан імунної системи. Мета дослідження – вияснити та порівняти особливості змін де-яких показників імунної системи та зясувати їх роль для патогенезу експериментального алергійного аль-веоліту та експериментального алергійного альвеоліту, поєднаного з експериментальною пневмонією. Ме-тоди. Експериментальні дослідження здійснювали на 67 морських свинках (самцях) масою тіла 0,18 - 0,22 кг. Мурчаків розподіляли на три групи: перша група — інтактні тварини — контроль (10); друга група (дослідна) — тваринки з експериментальним алергійним альвеолітом (ЕАА): на 7-у, 14-ту, 21 -у доби екс-перименту (27); третя група (дослідна) — морські свинки з поєднаною патологією ЕАА та експеримента-льною пневмонією (ЕП) також на на 7-у, 14-ту, 21-у доби експерименту (30). ЕП та ЕАА відтворювали за авторською методикою Регеди М.С. (2024). Декапітацію тварин проводиди за допомогою хлороформного наркозу у зазначені вище терміни експерименту. Результати. Отримані нами результати дозволяють стве-рджувати, що за умов розвитку експериментального алергійного альвеоліту, поєднаного з експеримента-льною пневмонією відбуваються доволі значні зміни зі сторони імунної системи. Це проявлялося знижен-ням рівня Т-лімфоцитів сироватки крові морських свинок як за умов розвитку експериментального алер-гійного альвеоліту так і експериментального алергійного альвеоліту, поєднаного з експериментальною пневмонією. Одночасно ці дві досліджувані патології супроводжуються активацією гуморальної ланки імунітету, що проявлялося підвищенням концентрацції В-лімфоцитів та ЦІК сироватки крові морських свинк у всі терміни досліджуваної патології. Також встановлено, що експериментальний алергійний аль-веоліт асоційований з експериментальною пневмонією викликає більш істотні розлади клітинної та гумо-ральної ланок імунітету. Висновок. Експериментальний алергійний альвеоліт, особливо в поєднанні з пне-вмонією, призводить до поступового пригнічення клітинної ланки імунітету (зниження Т-лімфоцитів) та активації гуморальної ланки (зростання В-лімфоцитів та ЦІК), причому поєднання альвеоліту з пневмо-нією викликає більш виражені імунні розлади, особливо на ранніх етапах розвитку патології.

Aim. Nitric oxide (NO) and the variants of the endothelial nitric oxide synthase gene (NOS3) in multiple sclerosis (MS) have become a focus of active scientific interest in recent years. The NOS3 gene is constitutively expressed in neuronal and epithelial cells. Moreover, the endothelial NO synthase enzyme (eNOS) activity, which plays a pivotal role in developing endothelial dysfunction, is regulated by variants of the NOS3 gene, including the 4a/b variant.
Objective. To evaluate the influence of the 4a/b variant of the NOS3 gene on the susceptibility to and progression of multiple sclerosis.
Materials and Methods. The study included 113 patients diagnosed with MS. Genotyping for the 4a/b variant of the NOS3 gene was performed using the polymerase chain reaction method.
Results. Our findings indicate that the presence of the 4bb genotype is associated with a reduced risk of developing MS, whereas the 4a allele of the NOS3 gene is linked to an increased risk. Clinical characteristic analysis revealed that patients with the 4ba and 4bb genotypes exhibited a significantly higher body mass index
(BMI) (p=0.007) than those with the 4aa genotype. Additionally, patients with the 4bb genotype were substantially more likely to experience a severe disease course (p=0.0489). Binary logistic regression analysis identified a gene-environment interaction between the NOS3 4a/b variant and BMI (p=0.037), suggesting a combined effect of these factors on MS progression.
Conclusions. The results underscore the significant and complex role of the NOS3 4a/b variant in the pathogenesis and progression of MS. Further investigation is warranted to deepen our understanding of the mechanisms underlying this genetic factor and its interplay with other contributing variables.
Keywords: multiple sclerosis, NOS3, 4a/b variant, genotype frequency, body mass
index, EDSS

This article presents the results of an original study conducted on a cohort of pediatric patients with multiple sclerosis (MS), with radiological biomarkers of the disease assessed. In addition to conventional magnetic resonance imaging (MRI) sequences, brain structure volumetry was performed using advanced MRI techniques. Brain MRI remains the primary imaging modality for MS. The examination includes standard MRI sequences—T1-weighted, T2-weighted, and post-contrast T1-weighted images—which are essential for diagnostic confirmation of MS in accordance with the 2017 revision of the McDonald criteria. Furthermore, MRI is the leading method for identifying MS exacerbations through post-contrast T1-weighted imaging, allowing clinicians to monitor disease progression. With the advancement of imaging technologies, more comprehensive diagnostic opportunities
have emerged, particularly in the context of MS, through the use of advanced modalities such as volumetric analysis of brain structures. The present study demonstrated a statistically significant reduction in thalamic volumes and increased hippocampal volumes in children with MS compared to the control group. Currently, there is no consensus regarding the routine application of advanced MRI methods for MS diagnosis and monitoring, particularly in pediatric populations. However, we believe that such techniques have the potential not only
to improve and expedite MS diagnostics but also to contribute to the prediction of disease trajectory.
Early and timely radiological assessment may enhance MS management and significantly improve the quality of life for both pediatric and adult patients.
Keywords: multiple sclerosis, children, neuroimaging, brain volumetry.

UDC 616.832-004.2-07:577.164.11:577.161.3

Introduction. Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system
characterized by demyelination and neurodegeneration. Emerging evidence suggests a potential role
of folate metabolism, vitamin D status, and MTHFR gene polymorphisms in MS pathogenesis and
progression. In populations without food fortification, such as Ukraine, these factors may be particularly
relevant, highlighting the need to study their interrelationships with clinical disease features.
Aim. To investigate the relationship between folate metabolism markers (homocysteine, folic acid, and
vitamin B12), vitamin D levels, MTHFR gene variants, and the clinical characteristics of disease progression
in patients with MS.
Materials and methods. This study assessed biochemical markers of folate metabolism (homocysteine,
folic acid, vitamin B₁₂), vitamin D levels, and the MTHFR rs1801133 genotype in 113 MS patients, with
in-depth biochemical analysis conducted in a randomly selected subgroup of 36 patients. Clinical and
demographic data were collected, and statistical analyses were performed to evaluate correlations
between biochemical, genetic, and clinical parameters.
Results. Patients demonstrated elevated median homocysteine levels and suboptimal concentrations of
folic acid, vitamin B₁₂, and vitamin D. Significant inverse correlations were observed between homocysteine
and folic acid levels, as well as between vitamin D levels and EDSS scores. Smokers had significantly lower
vitamin B₁₂ levels. Although the difference was not statistically significant, patients with the TT genotype
of MTHFR rs1801133 showed a trend toward lower folic acid levels. Homocysteine levels were highest in
patients with secondary progressive MS, indicating a possible link to disease progression.
Conclusions. Findings highlight the potential contribution of disrupted folate metabolism and vitamin D
deficiency to MS pathogenesis, particularly in populations lacking food fortification. These results
underscore the need for further research into vitamin-based interventions as possible strategies for
modifying disease course.
Keywords: folate metabolism, homocysteine, methylenetetrahydrofolate reductase, multiple
sclerosis, neurodegeneration, vitamin B₁₂, vitamin D