Background: Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths globally, accounting for approximately 85% of lung cancers. Although the level of diagnosis and treatment continues to improve, the patient’s prognosis is still unsatisfactory due to the high recurrence and metastasis rates. Searching for potential molecular markers is of great significance for early diagnosis, prognostic assessment and targeted treatment. Human aldehyde dehydrogenase 18 family member A1 (ALDH18A1) has been found to be associated with tumor proliferation and prognosis in a variety of cancers, but its expression and clinical significance in NSCLC are unclear. Aim: To verify the protein expression characteristics of NSCLC through immunohistochemical experiments on tissue chip, and provide theoretical basis for molecular diagnosis and targeted treatment of NSCLC. Materials and Methods: In this study, ALDH18A1 protein expression was determined in 80 cases of lung squamous cell carcinoma (LUSC), 52 cases of adenocarcinoma (LUAD), and adjacent tissues of combined tumors using TMA and IHC methods. Indirect IHC staining was performed on 4-μm-thick sections, and semiquantitative evaluation was performed based on the staining intensity and percentage of positive cells. ALDH18A1 expression was analyzed in relation to clinicopathological parameters (age, sex, TNM stage, clinical grade) and patient survival. Result: ALDH18A1 was highly expressed in the tumor tissues of 132 cases of LBCL, but was low or absent in the surrounding normal tissues. In LUSC, high ALDH18A1 expression was significantly associated with poor tissue differentiation (P<0.001), advanced TNM stage (P<0.001), distant metastasis (P=0.0327) and tumor size (P=0.0166). In LUAD, it was associated with poor tissue differentiation (P<0.001), advanced TNM stage (P<0.001) and tumor size (P=0.00302). According to Kaplan–Meier analysis, OS of patients with high ALDH18A1 expression was significantly shorter than that of those with low expression (LUSC: P=0.0014, LUAD: P<0.0001). The results showed that high ALDH18A1 expression was strongly associated with the infectivity of HLH and poor prognosis. Conclusion ALDH18A1 is highly expressed in NSCLC tissue and is related to tumor progression. It may serve as a potential molecular marker and treatment target, providing reference for the diagnosis and prognosis of NSCLC.

Background: Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer, and its incidence and mortality rates have long ranked among the highest of malignant tumors worldwide. Through bioinformatics analysis, this study identified the oncogene ALDH18A1, which is closely related to the development of NSCLC. Recent studies have shown that ALDH18A1 is highly expressed in various malignant tumors and participates in regulating biological processes such as cell viability and proliferation. However, its specific role and molecular mechanism in NSCLC remain unclear. Aim: To investigate the expression characteristics of ALDH18A1 in NSCLC cells and its effects on cell viability and proliferation. Materials and Methods: The expression levels of ALDH18A1 in various NSCLC cell lines and normal lung cells were detected by real-time quantitative PCR (qPCR) and Western blot. NSCLC cell lines with high ALDH18A1 expression were selected, and ALDH18A1 was knocked down using siRNA technology. The effects of ALDH18A1 downregulation on cell viability and proliferation were evaluated using CCK-8 assays and colony formation assays, and the experimental results were analyzed using statistical methods. Result: The expression level of ALDH18A1 in NSCLC cell lines was significantly higher than that in normal lung cells, and the expression was particularly significant in H1975 cells. Knockdown of ALDH18A1 expression significantly reduced the viability and proliferation capacity of NSCLC cells, and the difference was statistically significant (P<0.05). Conclusion ALDH18A1 is highly expressed in NSCLC cells, and its downregulation can significantly inhibit the viability and proliferation of tumor cells, suggesting that ALDH18A1 plays a pro-tumor role in the occurrence and development of NSCLC and has research value as a potential oncogene and therapeutic target.

Background: Metabolic syndrome (MetS) has been shown to be associated with multiple factors, including central obesity, insulin resistance, lipid metabolism disorders, and elevated blood pressure, thereby increasing the risk of cardiovascular disease and type 2 diabetes. In recent years, the prevalence of MetS has risen sharply worldwide, affecting about one-third of the global population, becoming a major public health concern. Although several studies on MetS have been conducted in Mongolia, research investigating the relationship between iron metabolism and MetS, particularly among men who are most affected, is limited. This formed the basis for the present study. Aim: To investigate selected indicators of iron metabolism in men with and without MetS. Materials and Methods: A total of 227 men aged 30-60 years from Ulaanbaatar were included in this study. Participants were classified into two groups: MetS (case group) and non-MetS (control group). According to the British Columbia “High Ferritin and Iron Overload – Investigation and Management” (2021) guidelines, serum ferritin levels were categorized into three groups: <300 ng/mL as normal ferritin, 300–600 ng/mL as hyperferritinemia, and >600 ng/mL as iron overload. Result: The mean age of the participants was 45.3±8.3 years. Based on the 2009 JIS criteria for MetS (five components), 38.8% (n=88) had MetS and 61.2% (n=139) were without MetS. According to the British Columbia guidelines, 46.7% (n=106) had normal serum ferritin, 33.9% (n=77) had elevated ferritin, and 19.4% (n=44) had iron overload. When serum iron-related proteins were analyzed by group, the ferritin levels ranged from 33.30 to 1330.00 ng/mL with a mean of 320.34 in the non-MetS group, and from 43.10 to 1044.00 ng/mL with a mean of 378.28 in the MetS group (F=3.957, Sig=0.049), indicating a statistically significant difference in ferritin levels between the two groups. Other iron metabolism indicators, including serum iron, transferrin saturation (TSAT%), Unsaturated iron binding capacity (UIBC), Total iron binding capacity (TIBC), and hepcidin, did not show statistically significant differences between groups. Conclusion Among the indicators of iron metabolism, only serum ferritin levels showed a statistically significant difference between men with and without MetS. Other indicators did not differ significantly, highlighting the need for further detailed investigation.

Background: The autonomic nervous system plays a curical role in the regulation of vital physiological functions, including cardiac rhythm, heart rate, and maintenance of blood pressure homeostasis. Previous studies have reported that autonomic nervous function gradually declines with aging, particularly after the age of 40, with an estimated reduction of 5-8% per decade. Globally, the prevalence of atrial fibrillation is rapidly increasing, and it is estimated that by 2050, approximately 72 million people in Asia will be diagnosed with atrial fibrillation, with nearly 3 million cases expected to develop ischemic stroke as a complication. Several risk factors, including arterial hypertension, obesity, alcohol consumption, and smoking, contribute to the development of atrial fibrillation, partly by disrupting autonomic nervous system regulation. Patients with atrial fibrillation have a 1.5-2-fold higher risk of mortality compared with the general population, and the lifetime risk of developing atrial fibrillation after the age of 40 is estimated to be approximately 25%. Aim: To assess autonomic nervous system dysregulation based on heart rate variability parameters among individuals aged 40 years and older. Materials and Methods: The stady was hospital-based case–control study was conducted among patients who received outpatient care and underwent 24-hour Holter electrocardiography (ECG) at Promedica Cardiology Hospital between October 2025 and February 1, 2026. A total of 70 participants were selected using a random sampling method. Of these, 31 patients diagnosed with paroxysmal atrial fibrillation were included in the case group, based on clinical records and Holter ECG findings. The control group consisted of 39 participants without atrial fibrillation. Autonomic nervous system regulation was evaluated using time-domain HRV parameters (rMSSD, pNN50) and frequency-domain parameters (LF, HF, and LF/HF ratio). Statistical analyses were performed using STATA version 15.0 A p-value of <0.05 was considered statistically significant. Result: Among the study participants, 37.1% (n=26) were male and 62.9% (n=44) were female. The mean age was 56.9±11 years (range: 40–79). Of the total participants, 44.2% (n=31) belonged to the paroxysmal atrial fibrillation group, while 55.8% (n=39) were included in the control group. A statistically significant difference in age and sex distribution was observed between the two groups (p=0.001). A significant association was identified between autonomic nervous system dysregulation and paroxysmal atrial fibrillation (p=0.001). In the paroxysmal atrial fibrillation group, increased pNN50, rMSSD values, and a decreased LF/HF ratio were observed, indicating impaired parasympathetic (vagal) activity. These alterations were associated with an increased risk of atrial fibrillation, with an odds ratio (OR) of 4.90 (95% CI: 1.98-12.14). No statistically significant differences in autonomic nervous system parameters were observed in the control group. Conclusion Autonomic nervous system dysfunction assessed through heart rate variability parameters may play a significant role in the development of atrial fibrillation. Holter ECG–based heart rate variability analysis could therefore be utilized as a clinical tool for early detection of paroxysmal atrial fibrillation, risk assessment, improved monitoring, and optimization of treatment strategies.

Background: According to the World Health Organization (WHO), 25–30% of the total population in developing countries are affected by metabolic syndrome (MetS). MetS is defined as a cluster of interrelated conditions encompassing abdominal obesity, arterial hypertension, hyperglycemia, and dyslipidemia, and constitutes a significant precursor to cardiovascular disease (CVD), cerebrovascular accident (stroke), and type 2 diabetes mellitus (T2DM). The global prevalence of MetS continues to rise in parallel with increasing rates of sedentary behavior and obesity. Morphological alterations associated with MetS are reflected in changes in anthropometric parameters that vary according to individual constitutional characteristics. Physical development is a dynamic process influenced by age, sex, occupational activity, living environment, and geographic-climatic conditions. In the Mongolian population, specific lifestyle patterns, climatic factors, and behavioral characteristics further amplify the risk of obesity, thereby contributing to increasing morbidity and mortality from T2DM and CVD. Although previous studies in Mongolia have examined the prevalence of MetS and its associated risk factors, data on anthropometric profiles of individuals with MetS remain limited. Therefore, establishing normative anthropometric reference values for individuals with MetS in the Mongolian population is of critical importance. Aim: To determine and compare selected anthropometric parameters between Mongolian males with metabolic syndrome and those without metabolic syndrome. Materials and Methods: A total of 227 males aged 30-60 years residing in Ulaanbaatar city were enrolled in this study. Participants were classified into two groups according to the 2009 Joint Interim Statement (JIS) diagnostic criteria: 88 males (38.8%) met the diagnostic criteria for MetS (case group) and 139 males (61.2%) did not (control group). Results: Comparisons of anthropometric measurements stratified by serum ferritin quartiles revealed statistically significant differences in body weight, waist circumference (WC), body mass index (BMI), waist-to-hip ratio (WHR), percentage body fat, fat mass, and skeletal muscle mass between the MetS and non-MetS groups (p<0.001). When anthropometric parameters were compared across serum ferritin strata, only percentage body fat showed a statistically significant elevation (p=0.037), while no significant differences were observed for the remaining parameters (p>0.05). Linear regression analysis indicated that BMI (beta=3.21, p=0.036) and WHR (beta=7.11, p=0.047) independently increased the risk of elevated serum ferritin levels by 3.2-fold and 7.1-fold, respectively. Conclusions 1. Anthropometric and hemodynamic parameters including BMI, waist circumference, waist-to-hip ratio, systolic blood pressure, and diastolic blood pressure were all significantly different between the MetS and non-MetS groups, whereas body height showed no statistically significant difference between the groups (F=0.002, p=0.962). 2. Serum ferritin concentration showed statistically significant weak positive correlations with waist circumference (r=0.20), BMI (r=0.19), waist-to-hip ratio (r=0.26), and body fat percentage (r=0.23) (p<0.01). Linear regression analysis identified BMI (β=3.21, p=0.036) and waist-to-hip ratio (β=7.11, p=0.047) as independent predictors associated with a 3.2-fold and 7.1-fold increased risk of elevated serum ferritin, respectively.

Background: Conventional methods for assessing exposure to environmental tobacco smoke rely mainly on questionnaires and biomarkers with short half-lives, such as urinary cotinine. In contrast, oral mucosal pigmentation may represent a visible, non-invasive biomarker of chronic exposure. However, its clinical and policy relevance, as well as its validity for screening purposes, remain insufficiently established. Aim: To summarize the evidence on the association between exposure to environmental tobacco smoke and oral mucosal pigmentation and to assess some confounding factors. Materials and Methods: We synthesized findings from observational studies that examined the association between environmental tobacco smoke exposure and oral mucosal pigmentation across all age groups. International electronic databases, including PubMed, Embase, Web of Science, and Scopus, were searched. Data were extracted on exposure–response relationships, measurement instruments, anatomical distribution of pigmentation, confounding by physiological pigmentation, and biochemical validation. The quality of included studies was assessed using the Mixed Methods Appraisal Tool (MMAT). A narrative synthesis was conducted, focusing on the biological plausibility of the biomarker, standardization of measurement, and its potential implications for screening and tobacco control policy. Results: Thirteen observational studies from seven countries, involving a total of 3,284 participants, met the inclusion criteria. Four studies reported a statistically significant association between duration of exposure and severity of pigmentation, while one cohort study showed that urinary cotinine levels increased with age among children. The Gingival Pigmentation Index and the Dummett Oral Pigmentation Index were the most commonly used assessment tools; however, methodological heterogeneity limited direct comparability across studies. The anterior gingiva was the most frequently affected anatomical site. Only a limited number of studies adequately controlled for physiological pigmentation, and skin color was identified as an important confounding factor. The pooled odds ratio was 2.35; however, the certainty of evidence was low due to the observational nature of the included studies. Conclusion Oral mucosal pigmentation may serve as a potential biomarker of long-term exposure to environmental tobacco smoke. Nevertheless, standardized assessment protocols, adequate control for physiological pigmentation, and validation against “gold-standard” biomarkers are required. If validated, this marker could be used for rapid identification of high-risk groups and incorporated into tobacco control policies.

Background: Passive smoking among children remains a serious public health concern, particularly because children’s ability to avoid household environmental tobacco smoke exposure is limited when parents smoke. In recent years, increasing scholarly attention has been given to oral mucosal pigmentation as a potential clinical sign of long-term passive smoking in children. However, no previous study has synthesized the available evidence on this topic. Aim: This systematic review and meta-analysis aimed to evaluate the association between passive smoking and oral pigmentation in children. Materials and Methods: A systematic search was conducted in international electronic databases, including PubMed, Scopus, Web of Science, and the Cochrane Library, in accordance with PRISMA guidelines. Observational studies assessing the association between passive smoking and oral pigmentation among children aged ≤18 years were included. Methodological quality was assessed using the Mixed Methods Appraisal Tool (MMAT). A random-effects meta-analysis was performed, and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Between-study heterogeneity was assessed using the I² statistic, and the certainty of evidence was evaluated using the GRADE approach. Results: Seven studies involving a total of 1,582 participants met the inclusion criteria. The meta-analysis demonstrated that passive smoking was significantly associated with an increased risk of oral pigmentation in children, with a pooled OR of 2.58 (95% CI, 1.35-4.95; p=0.004). Compared with children without exposure to passive smoking, those exposed to environmental tobacco smoke had an absolute risk increase of 17% (95% CI, 6.3%-23.9%). Subgroup analysis by assessment method showed a consistent effect among studies using the Gingival Pigmentation Index (GPI) (OR, 2.12; 95% CI, 1.58-2.84), whereas studies using the Dummett Oral Pigmentation Index (DOPI) showed a wider confidence interval (OR, 3.26; 95% CI, 0.68-15.54). According to the MMAT assessment, the included studies demonstrated adequate participant selection in 100% of cases, appropriate outcome measurement in 76.9%, and adequate control of confounding factors in 46.2%. Owing to the observational nature of the included studies, moderate heterogeneity, and the potential risk of confounding by physiological pigmentation, the certainty of evidence was rated as low according to GRADE. Conclusion Children exposed to environmental tobacco smoke had a significantly higher likelihood of oral mucosal pigmentation than unexposed children. These findings suggest that screening for oral mucosal pigmentation during pediatric oral examinations may serve as a non-invasive marker of passive smoking exposure and may provide visible clinical evidence to support counseling parents on smoking cessation and smoke-free household environments.

Background: Mongolia ranks first in the world for liver cancer incidence and mortality, with more than 95% of cases associated with hepatitis B virus infection. Healthcare professionals are considered a priority group for vaccination. Aim: To investigate the level of hepatitis B virus immunization among dental specialist physicians. Materials and Methods: This retrospective, observational, analytical cross-sectional study was conducted with approval from the Research Ethics Committee of the Mongolian National University of Medical Sciences (MNUMS). We analyzed serum test data from 76 dentists officially registered in the Dentistry residency program during the 2025–2026 academic year, assessing hepatitis B virus infection status and immunization levels. Statistical analysis of quantitative data was performed using SPSS version 27. Results: Data from 76 dentists were analyzed. The mean age was 28.5±6.2 years; by age group, 70% (n=53) were aged 20–29 years, 22.3% (n=17) were 30–39 years, and 7.8% (n=6) were over 40 years (p<0.05). By sex, 13.2% (n=10) were male (p>0.05). Among the study participants, 97.4% were HBV-negative with a mean age of 28.2±5.3 years (Median: 27.0, IQR: 24.0–31.0), whereas 2.6% were infected; the mean age of infected physicians was 43.5±2.1 years (Median: 43.5, IQR: 42.0–45.0), indicating a high and statistically significant occurrence of HBV infection in the age group over 40 years (Fisher’s exact test, p=0.05). When classified by immunity level, 29.2% (n=19) had anti-HBs levels below 10 mIU/mL (insufficient), 24.6% (n=16) had anti-HBs levels of 10–99 mIU/mL (weak), and 46.2% (n=30) had anti-HBs levels above 100 mIU/mL (adequate immunity); however, no statistically significant association was observed between age groups and protective antibody levels (Fisher’s exact test, p=0.892). Conclusion Among participants, the prevalence of hepatitis B virus infection was 2.6%, vaccination coverage was 85.5%, and anti-HBs antibody titers were adequate in 46.2%.

Background: Although a considerable number of oral health studies have been conducted among children in Mongolia, most have focused on dental caries in school-aged children, and data on non-carious oral conditions in preschool children remain scarce. Aim: To determine the prevalence of oral mucosal, gingival and traumatic dental conditions among preschool children in Ulaanbaatar. Materials and Methods: In this cross-sectional pilot study, 686 children from six randomly selected kindergartens in Ulaanbaatar underwent oral examination in accordance with the World Health Organization (WHO) 2013 guidelines, using the WHO Oral Health Assessment Form for Children. The main outcomes were oral mucosal changes, including pigmentation, gingival bleeding, dental trauma and dental erosion. Analyses were restricted to the 598 children with complete records for these outcomes, and frequencies, percentages and Wilson 95% confidence intervals (CIs) were calculated using this common denominator (n=598). Results: Of the 598 children analysed, 86 (14.38%; 95% CI 11.80–17.42%) had at least one of the four main conditions. Dental erosion was observed in 74 children (12.37%; 95% CI 9.97–15.26%), confined to the enamel in 45 (7.53%) and extending into the dentine in 29 (4.85%). Oral mucosal changes were recorded in 10 children (1.67%; 95% CI 0.91–3.05%), gingival bleeding in 7 (1.17%; 95% CI 0.57–2.40%) and dental trauma in 1 (0.17%; 95% CI 0.03–0.94%), whereas oral mucosal pigmentation was observed in 64 children (10.70%; 95% CI 8.47–13.44%). Of the 86 children with findings, 85 (98.84%) attended two of the six participating kindergartens. Conclusion When dental caries was excluded, dental erosion was the most prevalent condition among preschool children, whereas oral mucosal changes, gingival bleeding and dental trauma were observed in a small proportion of children. The concentration of these findings in two of the six kindergartens may reflect local demographic and socioeconomic factors, as well as differences in examination and recording practices. Future studies should therefore standardise examination criteria in advance and include a larger number of kindergartens.

Background: HepG2 cells are widely used as an in vitro model for investigating alterations in hepatic cellular metabolism. Studies evaluating the biological activities of plant-derived compounds using HepG2 cells have also increased. Strawberry (Fragaria orientalis), lingonberry (Vaccinium vitis-idaea), radish (Raphanus sativus), and blue honeysuckle (Lonicera caerulea L.) contain polyphenols, flavonoids, anthocyanins, and other secondary metabolites. The biological activities of these plants may vary depending on species, plant tissue, growing conditions, and extraction methods. Prior to evaluating the biological activities of plant extracts, it is essential to assess their cytotoxic effects on cells and determine appropriate concentrations for subsequent experiments. Therefore, evaluating the effects of plant extracts on the viability of HepG2 cells, a human hepatocellular carcinoma cell line, is of considerable importance. Aim: To evaluate the effects of aqueous and ethanolic extracts of strawberry, lingonberry, radish, and cultivated and wild blue honeysuckle on HepG2 cell viability and to determine concentrations exhibiting cytotoxic effects. Materials and Methods: A total of 18 plant extracts were prepared using water and ethanol as extraction solvents. The extracts were obtained from strawberry leaves, lingonberry leaves, radish, and the fruits, stems, and leaves of cultivated and wild blue honeysuckle. The extracts were subsequently dried. HepG2 cells maintained in the Cell Biology Laboratory of the Institute of Biomedical Sciences were revived, stabilized, and used for the experiments. The plant extracts were prepared at concentrations of 6.25, 12.5, 25, 50, 100, 200, and 300 μg/mL and used to treat HepG2 cells. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Cytotoxicity was defined as a reduction in cell viability of more than 30% compared with the control group. Results: The aqueous extract of cultivated blue honeysuckle and the ethanolic extracts of its fruits and stems maintained HepG2 cell viability above 70% across the concentration range of 6.25–300 μg/mL, indicating relatively low cytotoxicity. In contrast, the ethanolic extract of cultivated blue honeysuckle leaves reduced cell viability at higher concentrations. The aqueous and ethanolic extracts of fruits and stems of wild blue honeysuckle showed no apparent cytotoxic effects, whereas both aqueous and ethanolic extracts of its leaves reduced cell viability to approximately 65% at 300 μg/mL, indicating relatively higher cytotoxicity. Most aqueous and ethanolic extracts of strawberry, radish, and lingonberry maintained cell viability above 70% and showed no cytotoxic effects. The ethanolic extract of strawberry leaves reduced cell viability to approximately 63% even at the lowest concentration of 6.25 μg/mL; however, cell viability tended to increase with increasing extract concentration. Conclusion The effects of plant extracts on HepG2 cell viability varied depending on plant species, tissue type, extraction solvent, and concentration. Most extracts of strawberry, lingonberry, radish, and the fruits and stems of cultivated and wild blue honeysuckle exhibited relatively low cytotoxicity at concentrations ranging from 6.25 to 300 μg/mL. However, the ethanolic extract of cultivated blue honeysuckle leaves at 200 μg/mL and the aqueous and ethanolic extracts of wild blue honeysuckle leaves at 300 μg/mL reduced cell viability by more than 30%, indicating relatively higher cytotoxicity.