Introduction:
Cognitive decline is a growing public health concern in Brazil due to its rapidly aging population. According to the Brazilian Institute of Geography and Statistics (IBGE), individuals aged 60 and over represented 14.7% of the population in 2022, with projections indicating this figure will reach 25.5% by 2060. Epidemiological data suggest that up to 20% of Brazilians over 60 experience some form of cognitive impairment, with approximately 7% meeting the criteria for dementia (Alzheimer’s Disease International, 2021).

Methods:
A cross-sectional analysis was conducted using national health survey data (Pesquisa Nacional de Saúde, PNS, 2019) and secondary sources, including DATASUS and IBGE demographic projections. The prevalence rates of cognitive impairment were analyzed by age group, sex, region, and educational level. The statistical analysis included chi-square tests for categorical variables and logistic regression for risk factor associations.

Results:
The prevalence of self-reported cognitive decline increased significantly with age, affecting 4.1% of individuals aged 60–69 and 12.7% of those over 80. Women reported higher rates of cognitive complaints (9.8%) compared to men (6.3%). Lower educational levels were strongly associated with increased cognitive decline (OR = 2.3, 95% CI: 1.8–2.9). Regional disparities were evident, with higher prevalence in the North and Northeast regions.

Conclusions:
Cognitive decline among older adults in Brazil presents significant social and health system challenges. Educational attainment and regional inequality are key determinants of cognitive health. These findings highlight the need for targeted public health interventions, early screening programs, and greater investment in geriatric care infrastructure, particularly in underserved regions.

Peripheral neuropathy is a common complication of diabetes that can lead to balance and gait alterations, increasing the risk of falls among diabetic patients. This study explores whether blood glycated hemoglobin is associated with gait and postural abnormalities and the risk of falls in diabetic patients. Methods: Gait and postural parameters were assessed using a wearable inertial sensor placed in the lumbar region of the participants, while risk of falls was determined using the Tinetti Scale. Glycaemic control was evaluated by blood glycated haemoglobin concentration. Results: Spearman's rank correlation test showed that glycated haemoglobin was correlated with gait and postural parameters such as swing duration (p=0.023), the sway path along the antero-posterior axis during tests carried out with the eyes opened and feet in tandem (p=0.043), the sway path along the antero-posterior axis during tests performed with the eyes opened and feet closed together (p=0.034), and the sway area during tests performed with the eyes closed and feet in tandem (p=0.043). Moreover, higher levels of glycated haemoglobin in blood were associated with a higher risk of falls in diabetic patients (p=0.035). Conclusions: These results show associations between blood glycated haemoglobin and gait and postural parameters and the risk of falls in diabetic patients, underscoring the importance of glycaemic control to prevent neuropathic complications and their consequences in diabetes mellitus.

The formation of neutrophil extracellular traps (NETs) is a mechanism of innate immunity. Dysregulation of this process contributes to tissue damage in various pathologies. However, data on the role of NETosis in the pathogenesis of diabetic osteoarthropathy (DOA) remain extremely limited. This study aimed to evaluate the informativeness of a modified method for assessing NET formation using combined neutrophil activation in patients with diabetes mellitus (DM) and DOA. The authors modified a patented technique for evaluating NETs induced by a nonspecific antigenic stimulator—a microbial culture containing L. reuteri, L. acidophilus, L. rhamnosus, and B. longum —applied to neutrophils isolated from peripheral venous blood. Thrombin solution ("Renam") was used as an additional NETosis activator. Microslides were analyzed using combined microscopy techniques: transmitted light for neutrophil visualization and fluorescence emission (excitation 450–480 nm, emission ≥515 nm) for detecting extracellular and intracellular DNA stained with propidium iodide (PI).

Сomparative analysis revealed optimal parameters: PI concentration ≥0.1 mg/mL, probiotic preparation at 2.5×10^9 bacteria/mL, thrombin activity at 3 IU/mL, and a leukocyte suspension/activator ratio of 1:10. Interassay coefficients of variation in 10 experimental series with thrombin were 13.8% in a healthy donor and 12.5% in a DOA patient. Neutrophils from type 2 DM patients exhibited enhanced NET formation upon stimulation with both probiotics and thrombin compared to healthy donors (*p*=0.002 and *p*<0.001, respectively). Notably, neutrophils from DOA patients (Charcot foot) demonstrated more pronounced filamentous NET formation than those from diabetic foot patients without osteoarthropathy (*p*=0.011).

The developed method allows for assessing NET formation in response to nonspecific antigenic stimulation and characterizing potential risks of immunothrombosis progression in DOA.

The study was supported by the Russian Science Foundation (Grant No. 25-25-20206, https://rscf.ru/project/25-25-20206/).

Background. The Latin American–Mediterranean (LAM) genotype of Myobacterium tuberculosis is widespread in most regions of the world. Its LAM-RUS branch is endemic to Russia and Northern Eurasia and is frequently multidrug-resistant. Although geographically distant, the LAM-RUS strains are closely related in their 24-MIRU-VNTR profiles, which may reflect their relatively recent dissemination across this sparsely populated area of Northern Eurasia. Practically, this means that the international 24-locus MIRU-VNTR format has limited utility for subtyping LAM-RUS strains. Here, we evaluated seven additional hypervariable VNTR loci for their discriminatory power among LAM-RUS strains.

Methods. A sample of 133 M. tuberculosis LAM strains from different locations was subjected to spoligotyping (followed by comparison with the SITVIT2 database) and 24-locus MIRU-VNTR typing. Seven hypervariable VNTR loci (3820, 4120, 3232, 1982, 2136a, 3155, and 3336) were additionally genotyped. MIRU-VNTRplus.org and PAUP software were used for the phylogenetic analysis of the VNTR data, treated as discrete variables. The Hunter–Gaston Index (HGI) was used to assess the discriminatory power of individual loci and their combinations.

Results. Based on spoligotyping, 22 different spoligotypes were identified, of which SIT42 was the most prevalent (n=37), followed by SIT254 (n=26) and SIT252 (n=22). Thirty-locus typing revealed 14 clusters (2–15 isolates) and 58 unique profiles. The Hunter–Gaston Index (HGI) for the 30-locus set was 0.979. The HGI values for individual loci ranged from 0 (MIRU4, MIRU24, MIRU39, Mtub29) to 0.5595 (VNTR3820) and 0.6165 (MIRU40). The combined discriminatory power of the 11 most polymorphic loci was 0.968 (13 clusters of 2–17 isolates; 67 unique profiles), which was nearly equivalent to that of the full 30-locus VNTR set.

Conclusions. This optimized 11-locus panel provides sufficient discriminatory power for LAM genotype strains and could serve as a cost-effective tool for primary epidemiological surveillance of this clinically important M. tuberculosis lineage.

Introduction. The Haarlem genotype of Mycobacterium tuberculosis is spread across many regions of the world. Its strains exhibit interesting pathogenic properties in mouse and macrophage models. Spoligotyping remains a classical method for Haarlem detection, but fails to reliably classify strains with abridged spoligoprofiles. Here, we developed and validated a real-time PCR (RT-PCR) assay for robust identification of the Haarlem genotype.

Materials and methods. M. tuberculosis genotyping was performed using spoligotyping with subsequent comparison against the international SITVIT2 database. Whole-genome sequencing was performed on HiSeq4000. For RT-PCR, we used LNA probes and the RotorGene thermal cycler.

Results. Primers and LNA probes were designed to target a previously reported Haarlem-specific mutation in Rv0282 (Shitikov, Bespiatykh, 2023). The method was optimized using DNA from Haarlem and non-Haarlem strains with available whole-genome sequences. The RT-PCR assay was tested on a collection of 293 isolates from the European and Asian parts of Russia, Belarus, Bulgaria, and Vietnam, previously characterized by spoligotyping and defined as Haarlem, with some strains classified as "unknown genotype" in SITVIT2. Isolates of other genotypes (Beijing, LAM, Ural, EAI) were also included as controls. Among Russian isolates, spoligotyping identified 39 as Haarlem and 35 as “unknown family”. The RT-PCR assay reclassified 10 of these unknown strains with truncated spoligoprofiles (SIT46, SIT237, and SIT1177) as Haarlem. For Belarusian isolates, spoligotyping detected only one Haarlem strain alongside six “unknown family” strains, whereas RT-PCR assigned all seven to Haarlem. All Haarlem isolates from Bulgaria (n=8; SIT47, SIT50) and Vietnam (n=1; SIT50) were correctly and concordantly confirmed by both methods.

Conclusions. The developed RT-PCR assay provides reliable detection of the Haarlem genotype, demonstrating that its true prevalence in certain regions is higher than previous spoligotyping-based estimates. These findings highlight the need for cautious interpretation of truncated spoligoprofiles, particularly those with extensive spacer deletions, in epidemiological studies of M. tuberculosis.

Background. In recent years, there has been an increase in acute allergic reactions (AAR), including anaphylaxis (AF), worldwide. AAR is based on certain clinical signs, but differential diagnosis often requires the use of additional diagnostic tests that can not only confirm the severity of the allergic reaction and its severity, but also predict its development. In this regard, the aim of our study was to examine the levels of tryptase, platelet activating factor (PAF), the enzyme acetylhydrolase of PAF (PAF-AG), and the content and activity of angiotensin-converting enzyme (ACE) in the blood serum of children with AAR.

Methodology. This study was conducted at pediatric hospitals in Belarus. A total of 60 children (average age 9.2 years) with AAR in the form of acute urticaria, angioedema, or their combination, as well as AF, were included in this study. The control group included 18 conditionally healthy children (average age 8.7 years). Measurements of tryptase, FAT, FAT-AG, and ACE concentrations were performed using enzyme immunoassay. ACE activity was studied spectrophotometrically using the Elabscience ACE Activity Assay Kit. Differences were considered statistically significant at p<0,05 and were analyzed using the Mann-Whitney U test.

Results. The results of our study showed that the median values of the levels of tryptase, PAF, and PAF-AG in the blood serum of children significantly increase with the development of AAR (in 2, 1.5, and 2.9 times, respectively), and correlate with the severity of AAR. In addition, these rates were higher in the group of children with AF compared to children without AF. The levels and activity of ACE in children with AAR also tended to increase relative to the control, but this increase was insignificant.

Conclusion(s). In conclusion, tryptase, PAF, and PAF-AG levels may act as potential biomarkers for the development of AAR in children.

Background. MicroRNAs are a class of small non-coding RNAs that perform important functions in regulating gene expression. Numerous data show that abnormal expression of microRNAs is observed in people with various oncopathologies. Platelet-derived microvesicles (PMVs) have been shown to carry microRNAs targeting oncogenes and tumor suppressor genes. MicroRNA-27 plays an important role in oncogenesis, proliferation, tumor cell metabolism, and chemotherapy resistance and also regulates the tumor immune response and the epithelial–mesenchymal transition. In this study, we examined the expression levels of miRNA-27 in PMVs from breast cancer (BC), lung cancer (LC), and kidney cancer (KC) patients before and after surgery.

Methodology. A total of 30 patients, 10 with breast cancer, 10 with lung cancer, and 10 with kidney cancer, and 10 clinically healthy individuals were involved in this study. All of the patients were subject to radical surgical treatment. PMVs were isolated from washed thrombin-stimulated platelets through sequential centrifugation. mRNA was extracted using the phenol–chloroform method. Synthesis of complementary DNA (cDNA) and the PCR analysis were performed using the miRCURY LNA miRNA PCR Starter Kit (Qiagen).

Results. The results indicated that the PMVs from all of the patients with various oncopathologies exhibited significantly reduced expression of microRNA-27 in comparison to that in the healthy donors. Namely, in BC, the median expression level of microRNA-27 was 6.4 times lower; in LC, it was 2.5 times lower; and in KC, it was 4.6 times lower. Post-surgery, the expression of microRNA-27 in the patients with BC and LC did not differ from the control values; however, in KC, it was drastically reduced by 3.5 times.

Conclusion(s). Consequently, our data suggest that platelet miRNA-27 may act as a potential diagnostic and prognostic biomarker for BC, LC, and KC; however, additional research with a larger sample size is required.

This work was supported by grant B23-RSF162 and grant 23-45-10039.

Background: Asthma is a prevalent chronic disease with significant economic and health burdens worldwide. Its progression involves key hallmarks such as inflammation and airway remodeling, mediated by multiple inflammatory biomarkers and pathways. Despite the availability of potent therapeutic options, many patients continue to suffer from uncontrolled asthma. The plasminogen activator inhibitor-1 (PAI-1) signaling pathway plays a critical role in asthma exacerbation and remodeling, with elevated PAI-1 levels linked to disease progression. Bioactive compounds are increasingly studied for their potential in asthma management, and anthocyanins (ACNs), with promising anti-inflammatory properties, are among these novel compounds.

Methods and Findings: This comprehensive review explores the potential of ACNs in managing asthma-related inflammation and modulating PAI-1 levels to influence airway remodeling. ACNs have shown promise in asthma management, with epidemiological studies associating higher ACN intake with a lower risk of asthma and improved lung function. Preclinical models demonstrate ACNs’ effectiveness in reducing inflammatory cytokines, chemokines, and signaling pathways related to asthma. Limited human trials suggest ACNs may improve symptom control and lung function. While no direct evidence links ACNs to PAI-1 reduction in asthma, studies in other chronic conditions indicate their ability to reduce PAI-1 levels, supporting their potential role in asthma management. This highlights a promising avenue for further exploration into their effects on airway remodeling.

Conclusion: Preliminary evidence suggests ACNs may be effective as an adjunct to reduce inflammation and improve symptom control. However, the lack of robust human interventional studies remains a significant gap. Future research should focus on establishing direct evidence of ACNs’ impact on PAI-1 levels and airway remodeling in asthma.

Background:

Emerging infectious diseases (EIDs) pose a significant global threat, with human-driven biodiversity loss increasingly recognized as a pivotal factor. Recent environmental disruptions are shaking up wildlife populations, altering host-pathogen interactions, and raising the risk of emerging diseases. However, the root causes linking biodiversity loss to EID emergence remain poorly understood. This research investigates the relationship between biodiversity loss, climate change, and infectious disease outbreaks using statistical methods, data analytical tools, and machine learning (ML) algorithms, such as survival analysis and Bayesian networks for predictive modeling.

Methods:

A multi-variant approach is proposed, integrating epidemiological data, bio-ecological modeling, and statistical data analyses. Biodiversity and disease incidence data are obtained from open-source databases such as Global Biodiversity Information Facility (GBIF) and Centers for Disease Control and Prevention (CDC). Survival analysis methods like Kaplan-Meier and Cox models assess the timing of disease outbreaks in the regions of human-driven biodiversity loss. Bayesian networks infer probabilistic relationships between environmental degradation, species richness, and zoonotic transmission. Machine learning algorithms further refine predictive models and computations for high-risk dynamics.

Results:

It is proposed that in the preliminary analyses, a strong correlation between biodiversity loss and increased EID incidence can be indicated, particularly in focused biodiversity regions. Survival models can reveal accelerated disease emergence in areas with rapid species decline. Overall, this research aims to identify high-risk areas that will support the development of an early-warning system.

Conclusion:

The main highlight of this research is to provide quantitative evidence linking biodiversity loss to infectious disease outbreaks, emphasizing the urgent need for integrated conservation and public health strategies. Findings will inform policy interventions to mitigate zoonotic risks and enhance disease surveillance systems in biodiversity-sensitive regions. In short, the proposed study will use a combination of systematic literature reviews, large-scale statistical analysis, and ecological modeling to explore diseases.

Background: In the pediatric population, pneumonia stands as the prevailing cause of mortality. The simultaneous presence of hypoalbuminemia and iron deficiency anemia presents specific difficulties in the treatment of pediatric pneumonia. Objectives: (1) Determine the proportion of coexistence of both hypoalbuminemia and iron deficiency anemia. (2) Evaluate the association between the coexistence of hypoalbuminemia, iron deficiency anemia, and pneumonia in children faged between 2 months and 5 years old at Ca Mau Obstetrics and Pediatrics hospital in 2022-2023. Research subjects and methods: A cross-sectional descriptive study was conducted on 177 young patients, aged 2 months to 5 years old, who were diagnosed with pneumonia. The diagnosis of pneumonia was based on the WHO diagnostic criteria for pneumonia in children under 5 years old. The children had the following symptoms: a cough and/or difficulty breathing and/or fever accompanied by rapid breathing or chest indrawing; tachypnea compared to age according to the World Health Organization; or small moist rales, whistling rales, or snoring rales noted in the lungs via an examination, or a cardiopulmonary X-ray showing pneumonia. Results: The percentage of male patients was 56.5%. The average age was 22.5±15.82 months old. The coexistence of hypoalbuminemia and iron deficiency anemia was found in 14.1% of cases. Children who had hypoalbuminemia and iron deficiency anemia were more likely to experience severe pneumonia, with a rate of 36% compared to 7.9% in the control group. Twenty-four percent of the participants in the study used a greater amount of antibiotics, which was significantly higher than the control group's rate of 3.9%. More than half of the patients required hospitalization for more than a week. Conclusion: The consequence of the simultaneous presence of both hypoalbuminemia and iron deficiency anemia is an exacerbation of pneumonia severity requiring a higher quantity of antibiotics for treatment.