There is a global need to discover effective anti-cancerous compounds from natural sources. Cultivated wheat cells can be a valuable source of non-toxic or low toxic plant-derived polysaccharides. In this study, we evaluated the anti-cancer ability of seven fractions of wheat cell culture polysaccharides (WCCPSs) in the HCT-116 colon cancer cell line. Almost all (6/7) fractions had an inhibitory effect on the proliferation of colon cancer cells, and two fractions (A-b and A-f) had considerable therapeutic indexes. The WCCPS fractions induced cell cycle arrest in the G1 phase and induced different rates of apoptosis (≤48%). Transmission and scanning electron microscopy revealed that WCCPS fractions caused apoptotic changes in the nucleus and cytoplasm, including damage to mitochondria and external morphological signs of apoptosis. In addition, the WCCPSs induced an increase in the levels of Bax, cytochrome c, and caspases 8 and 3, indicating that cell death progressed through intrinsic and extrinsic pathways of apoptosis. Furthermore, some fractions caused a significant decrease of c-Myc, b-catenin, NFkB2, and HCAM (CD 44) levels, indicating enhanced cell differentiation. Thus, for the first time, our results provide a proof of concept of the anti-cancer capacity of WCCPS fractions in colorectal cancer.

Natural polysaccharides (PSs) have shown inhibitory effects on differentiated cancer cells (DCCs), but their activity against cancer stem cells (CSCs) remains poorly understood. Here, we report that PSs from wheat cell cultures (WCCPSs) inhibit the proliferation of both DCCs and CSCs derived from HCT-116 colorectal cancer cells. Among them, NA and DC fractions showed the strongest anti-CSC activity. NA, rich in xylose, was effective at lower concentrations, while DC, enriched in xylose and galacturonic acid (GalUA), exhibited higher potency, with a lower IC₅₀ and preferential activity against CSCs at higher doses. WCCPSs reduced β-catenin levels, and some fractions also downregulated Ep-CAM, CD44, and c-Myc. Notably, DC increased caspase-3 without inducing cytochrome C and caspase-8 overexpression, suggesting a mechanism promoting CSC differentiation rather than apoptosis. Correlation analysis linked xylose content to reduced c-Myc expression, and GalUA levels to increased caspase-3. These results suggest that WCCPS bioactivity may be related to their monosaccharide composition. Overall, our findings support the potential of wheat-derived PSs as CSC-targeting agents that suppress self-renewal and promote differentiation, offering a promising approach to reduce tumor aggressiveness and recurrence.

Introduction: Bronchopulmonary dysplasia (BPD) remains the most significant complication of extreme prematurity, affecting long-term respiratory outcomes. Because current diagnostic criteria identify only established lesions at 36 weeks postmenstrual age, early non-invasive biomarkers are needed. This pilot study aimed to identify a candidate salivary miRNA panel associated with BPD risk and to explore its pathogenetic relevance through in silico analysis. Methods: Saliva was collected from 20 preterm infants (10 with BPD and 10 controls), and miRNA expression was profiled using the GeneChip™ miRNA 4.1 Array Plate. Discriminatory performance was explored by ROC analysis within this discovery cohort, together with power and Spearman correlation analyses. Results: Expression of hsa-let-7b-5p, hsa-let-7c-5p, and hsa-miR-4454 was significantly elevated in the BPD group (p < 0.05, log₂FC ≥ 1.0), with no significant correlation with gestational age or birth weight. Bootstrap-corrected AUC values ranged from 0.905 to 0.937 and were supported by leave-one-out cross-validation. All three miRNAs showed very large effect sizes exceeding the minimum detectable effect at 80% power. Conclusions: In this pilot study, salivary miRNAs represent a hypothesis-generating candidate biomarker signal for BPD that requires external validation in larger, independent cohorts before any diagnostic or prognostic application can be considered.

Aim: To evaluate the prevalence of post-infection fatigue (PVFS) over one year after COVID-19. Material and methods: 165 people who had COVID-19 more than a year ago were interviewed. A Fatigue Assessment Scale was used to assess the degree of fatigue. Chemiluminescent analysis was carried out to detect antibodies to Epstein-Barr Virus (EBV) antigens. For statistical analysis Fisher's exact test and Spearman correlation were conducted. Results: Among people with PVFS, there were 4.1 times more women than men (80.4% vs. 19.6%), people over 45 years old (76%), and people who needed hospitalization for COVID-19 (76%). The average fatigue duration was 573±18,3 days. Among individuals without PVFS, there were significantly more individuals under the age of 45 compared with the group of individuals with PVFS (40% and 24%, respectively, p=0.007) and there were significantly more individuals who did not need hospitalization compared with the group of individuals with PVFS (52% vs. 24%, p=0.005). EBV reactivation was determined in almost half of the individuals with PVFS (48%), while none of the individuals without PVFS had EBV reactivation. A statistically significant negative mean correlation was found between the duration of PVFS and the severity of PVFS (r=-0.357, p=0.007). A statistically significant negative correlation was found between the PVFS duration and the PVFS severity (r=-0.357, p=0.007). Conclusion: PVFS is a prevalent symptom after COVID-19. The duration of PVFS can reach and not be limited to 1.5 years. PVFS is more typical of women, people over 45 years of age and people who have had moderate and severe COVID-19. Over time, the severity of PVFS decreases. Key words: COVID-19, post-infection fatigue, Epstein-Barr virus

Introduction. Brucellosis remains one of the most widespread and underdiagnosed zoonotic infections, with over 500,000 new human cases annually and continued endemic circulation in livestock. Brucella melitensis, B. abortus, B. suis, and B. canis are the key pathogenic species causing chronic disease with nonspecific clinical symptoms. Brucella antigens are central to the pathogenesis and immune response, yet current diagnostic tests lack sufficient specificity, and no licensed human vaccine is available. This highlights the urgent need for more accurate antigen-based tools for both diagnosis and prevention. Aim. To review and evaluate the main Brucella antigens with proven or potential diagnostic and vaccine value, focusing on their structural features, immunogenicity, and applicability in translational research. Search strategy: A systematic review was conducted following PRISMA guidelines. Literature searches were performed in PubMed, Scopus, and Web of Science (2018–2025) using predefined keywords related to Brucella antigens, diagnostics, and vaccine development. After multi-stage screening of titles, abstracts, and full texts, 106 studies were included in the final analysis, as illustrated in the PRISMA flow diagram. Results. Outer membrane proteins (Omp16, Omp19, Omp25, Omp31), periplasmic proteins (BP26, Cu/Zn-SOD, L7/L12), heat shock proteins (Hsp60, Hsp70), and Type IV secretion system proteins (VirB) demonstrate distinct immunogenic profiles. Among them, L7/L12, Omp19, and SOD show the highest promise in terms of serological sensitivity and protective immune stimulation. A subset of these antigens is currently being explored as part of recombinant subunit vaccine formulations. Conclusion. Molecularly defined Brucella antigens offer tangible opportunities to improve human brucellosis diagnostics and support the rational development of safer, targeted vaccines. Their documented immunological relevance justifies further preclinical evaluation and standardization in applied immunodiagnostics. Введение. Бруцеллез остаётся одной из наиболее распространенных и недодиагностируемых зоонозных инфекций, с более чем 500 000 новых случаев среди людей ежегодно и устойчивой энзоотией среди сельскохозяйственных животных. Brucella melitensis, B. abortus, B. suis и B. canisявляются основными патогенными видами, вызывающими хронические заболевания с неспецифическими клиническими проявлениями. Антигены Brucella играют ключевую роль в патогенезе и формировании иммунного ответа, однако существующие методы диагностики недостаточно специфичны, а лицензированной вакцины для человека до сих пор не существует. Это подчёркивает необходимость создания более точных антиген-ориентированных средств диагностики и профилактики. Цель. Провести обзор и оценку основных антигенов Brucella spp., обладающих подтвержденной или потенциальной диагностической и вакцинной значимостью, с акцентом на их структурные особенности, иммуногенность и прикладную ценность. Стратегия поиска: Систематический обзор проведён в соответствии с рекомендациями PRISMA. Поиск литературы выполнен в базах PubMed, Scopus и Web of Science за период 2018–2025 гг. с использованием заранее определённых ключевых слов, связанных с антигенами Brucella, диагностикой и разработкой вакцин. После многоэтапного отбора по заголовкам, аннотациям и полным текстам в итоговый анализ было включено 106 исследований, что отражено на схеме PRISMA. Результаты. Наружные мембранные белки (Omp16, Omp19, Omp25, Omp31), периплазматические белки (BP26, Cu/Zn-SOD, L7/L12), белки теплового шока (Hsp60, Hsp70) и компоненты системы секреции типа IV (VirB) демонстрируют разную степень иммуногенности. Среди них белки L7/L12, Omp19 и SOD обладают наибольшим потенциалом как серологические маркеры и компоненты вакцинных конструкций. Часть этих антигенов рассматривается в составе рекомбинантных субъединичных вакцин. Заключение. Молекулярно охарактеризованные антигены Brucella открывают реальные перспективы для совершенствования диагностики и разработки целенаправленных и безопасных вакцин против бруцеллеза человека. Их иммунологическая значимость обосновывает необходимость дальнейшей доклинической оценки и внедрения в прикладную иммунодиагностику. Кіріспе. Бруцеллез – жыл сайын 500...

Periodontitis is epidemiologically associated with oral squamous cell carcinoma (OSCC), but the tissue-cell states shared by the two diseases are unknown. We integrated seven public droplet-based scRNA-seq datasets into an atlas of 498,185 cells from 111 oral mucosal samples using scVI/scANVI, benchmarked with scIB. Each disease was compared only with matched control tissue, using patient-level analyses. Both diseases expanded activated inflammatory and matrix fibroblast states. Activated and resting fibroblasts differed in a similar way in both diseases (ρ = 0.53; patient-bootstrap 95% CI 0.42–0.57), also within lesional tissue (ρ = 0.51). Disease-versus-control fibroblast responses, however, were only weakly shared (ρ = 0.24) and not within the oral cavity, so this similarity reflects a generic activated-stroma phenotype rather than a disease-specific fibroblast programme. Endothelial and mural responses were shared more strongly, whereas immune responses diverged. B/plasma-cell expansion was the only abundance change credible in both diseases. Periodontitis showed classical-monocyte influx and a lower share of C1Q+ macrophages. TREM2+ lipid-associated macrophages rose from leukoplakia to carcinoma, but their gain over tumour-adjacent tissue appeared in only one of two cohorts. SPP1–CD44 signalling passed significance thresholds only in OSCC. This cross-sectional study is hypothesis-generating and does not show causation.