BACKGROUND: Bladder cancer is a cancer of significant morbidity and mortality in the worldwide. It is the second most common urological cancer in Mongolia. It is important to understand the risk factors of bladder cancer.We evaluated the association of smoking, alcohol intake, body mass index and other potential risk factors with bladder cancer incidence in Mongolians.MATERIALS AND METHODS: We analyzed data from a case-control study (116 histologically confirmed bladder cancer cases and 300 cancer-free healthy, age, gender-matched controls). All participants signed the consent form andfilled out the structured questionnaire including cigarette smoking, BMI, chronic urinary disease andalcohol drinking etc. Using logistic regression we estimated the covariate-adjusted odds ratio (OR) and95% confidence interval (CI) of the associations.RESULTS: Mean age of the patients with bladder cancer was 56±10.5 years and 79.3% male and 20.7% female.Cigarette smoking, history of urinary tract diseases and body mass index were associated with an increased risk of bladder cancer OR 6, 48 (95% CI 1, 61-1, 70), OR 80 (95% CI 1, 48-1, 93) and OR=9.8 (95% CI 2.32-2.91) respectively but not alcohol drinking OR 0, 26 (95% CI 1, 56-1, 66).CONCLUSIONS: The results suggest that cigarette smoking, history of urinary tract diseases and body mass indexincreased risk of bladder cancer in Mongolian patients.

IntroductionThe p53 gene is frequently mutated in various forms of human cancers. The p53 signaling pathway isactivated by endogenous and exogenous stress signals and induces growth arrest, cellular senescenceand apoptosis. A common polymorphism occurs at codon 72 of the p53 has been demonstrated that itmight be associated with bladder cancer risk. However, results of researches related to this topic werecontroversial and more investigations and samples size needed.GoalTo evaluate TP53 Arg72Pro polymorphism in Mongolian patients with bladder cancer.Materials and MethodWe evaluated TP53 Arg72Pro polymorphism in DNA samples from 82 patients with bladder cancerand 82 age and gender matched healthy subjects using polymerase chain reaction-based restrictionfragment length polymorphism. All enrolments of this study were Mongolians. The association betweeneach genotype of TP53 Arg72Pro and bladder cancer risk was examined by the odds ratio and 95%confi dence interval, using logistic regression analysis. The early age onset of bladder cancer patientswas also evaluated among different genotypes of TP53 Arg72Pro.ResultsThe proportion of the polymorphism of TP53 Arg72Pro were RR 53.7% (n=44); PR 34.1% (n=28); andPP 12.2% (n=10) in the bladder cancer patients, whereas RR 52.4% (n=43); PR 28% (n=23); and PP19.6% (n=16) in healthy controls. The PR genotype increased the risk of bladder cancer (OR1.189;95% CI 0.42-0.75; p=0.997) in Mongolian people, whereas PP genotype protected from the cancer(OR=0.610; 95% CI 0.22-0.44, p=0.998) compared to the RR, respectively, however signifi cance isweak. Moreover, there was no association between each genotype of TP53 Arg72Pro (RR=52; PR=54;PP=58) and early onset of bladder cancer in the Mongolian population.Conclusion: Our result indicates that the PR genotype tends to increase the risk of bladder canceramong Mongolians. RR genotype of TP53 Arg72Pro is more prevalent among Mongolians.

BACKGROUND:The mouse double minute 2 (MDM2) is a negative regulator of the p53 tumor suppressor protein.Overexpression of MDM2 is associated with poor survival and is a useful predictive factor for poor prognosisin various cancers in human. Studies revealed a genetic polymorphism located in intron 1 of the MDM2gene, MDM2-SNP309, (a change from T to G) is main functional polymorphism and important to developtumors. However, inconsistent associations between the MDM2-SNP309 and the risk or early onset ageof human different cancers have been reported worldwide. These conflicting results may have dependedon different patient subgroups and ethnicities studies. We studied the association of the MDM2-SNP309polymorphism andbladder cancer in Mongolian patients for the first time.OBJECTIVE:To investigate association between MDM2-SNP309 and the risk bladder cancer or early onset age of thecancer in Mongolian patients.MATERIALS AND METHODS:We genotyped MDM2-SNP309 in 44 patients with bladder cancer and 44 age and gender matched healthycontrols among Mongolian people.Genomic DNA was extracted from whole blood samples by the standardmethod of Qiagen mini blood DNA extraction kit (Qiagen Inc., Valencia, CA) and PCR amplification wasperformed using 100 ng genomic DNA template according to manufacturer’s protocol (Invitrogen, Carlsbad,CA). MDM2 SNP309 genotyping was carried out by restriction fragment length polymorphism assay.RESULTS: The allele frequencies of MDM2 SNP309 in the 44 bladder cancer patients were wild-type (T/T) 27.3%,homozygous (G/G) 34.1% and heterozygous (T/G) 38.6% whereas in the control cases were wild-type(T/T) 29.5%, homozygous (G/G) 20.5% and heterozygous (T/G) 50.0%. The proportion of homozygous(G/G) genotype was higher for bladder cancer cases than for healthy controls. Compared to the low-risk(wild type) genotype, an increased risk association with bladder cancer was shown for the GG genotype(OR=2.0, 95% CI=1.03-1.84). There is also a significant difference in median age onset of bladder cancerbetween GG low and high risk genotypes T/T and T/G (p=0,003)( p=0.0001), respectively (Figure2).CONCLUTION: The current sample data suggests that MDM2 SNP309 GG genotype may be associated withthe risk of bladder cancer as well as an earlier age onset in Mongolian patients with bladder cancer.

Background: Studying the human embryonic and fetal organ systems development patterns and determining their quantitative indicators is of scientific and practical importance in medicine and health in every nation.
Distortions and pathologies during the development of the embryo are the causes of congenital disabilities. Among the congenital malformations, facial malformations are the 3rd place, including cleft lip and palate in 70% and Srouzon's syndrome in 30%. In addition, abnormalities due to changes in the size, shape, and position of the jaw are also mentioned in the 2021.04.21 issue of Morphology magazine in the study "Morphometric parameters of the bones of the skull and face during the development of newborns and fetuses". In our country, Ariuntuul G (2005) determined that cleft lip and cleft palate occur at 0.76/1000 or 1 in 1314 live births, while Ayanga G (2012) found that it occurs at 1 in 1072 live births or 0.93/1000. Moreover, the eye cup dimensions of Mongolian fetuses aged 16 36 weeks have a positive linear relationship with the gestational age determined using ultrasound by Nandintsetseg B (2015) et al. Compared with the other countries, the eyecup is slightly wider, and the outer edge distance is similar, whereas the inner edge distance is shorter. Purpose: To summarize research work and determine the embryonic development of bones involved in the formation of the face and facial parts, the period of bone formation, the point of ossification, and the period of formation. Methods: During fetal development, human organ systems grow and develop at different rates but in a particular relationship. This feature of growth and development is also clearly observed in the structure of the head and facial bones, and the results of researchers who have studied this aspect are selected in the articles. Results: Embryonic and fetal development of bone are clinically significant not only from the point of view of its morphogenesis but also from the point of view of congenital disabilities. Conclusion In the analysis of the sources, most of the works on the prenatal period of the development of the same body have studied the development of specific structures of the face and facial area, such as the palatine bones and nasal bones, or have generally covered the development of particular systems in the embryo and fetus, and face, there are relatively few works that show the entire dynamics of growth and development of facial bones.

Background: Tuberculosis (TB) is a preventable and usually curable disease. Yet in 2022, TB was the world’s second leading cause of death from a single infectious agent, after coronavirus disease (COVID-19)1. Aim: By reviving strains isolated at specific years over a 10-year interval and performing next-generation sequencing, we can analyze their strain genotype, epidemiology, drug resistance, and dynamicsTherefore, this study was conducted to examine the historical trends and dynamics of strain genotype, variants, and drug resistance of tuberculosis preserved in the culture bank. Materials and Methods:: Using a retrospective, laboratory-based research approach, 200 strains were randomly selected from over 1,000 diagnostic isolates preserved in the NTRL culture collection from 2010 and 2020. Whole-genome sequencing (WGS) was performed using GridION from Oxford Nanopore Technologies (ONT, Oxford, UK) to analyze these strains. The FastQ file was submitted to the International Mycobacterial Database. Strain genotypes, subtypes, gene mutations of drug resistance, and resistance profiles were identified using TBprofiler, MTBseq, IQ-Tree (version 1.6.12), and EPI2me software. Results: Of the tuberculosis strains selected for the study, 66.5% were from eight out of nine districts of Ulaanbaatar, while 33.5% were sampled from 16 out of 21 provinces. Out of the strains analyzed, 83.9% (95% CI 78.7–89.1) belonged to lineage 2 or the Beijing genotype, while 16.1% (95% CI 10.9–21.3) were lineage-4 or Euro-American genotype. While the proportion of Beijing lineage strains was slightly higher and the Euro-American lineage strains slightly lower in rural populations compared to urban populations, the difference in strain distribution between urban and rural areas was not statistically significant (p=0.485). Among the Beijing lineage strains, only the modern Beijing sublineage (100%) was identified. In contrast, the Euro-American lineage exhibited various sublineages: 4 (0.5%), 4.5 (1%), 4.1.2.1 (Haarlem, 3%), Latin American-Mediterranean (LAM, 7.5%), mainly T (3.5%), and S type (0.5%). Notably, the proportion of Lineage 2 strains increased from 80% in 2010 to 86% in 2020. The overlap of the confidence intervals for 2010 (72.16%–87.84%) and 2020 (79.20%–92.80%) indicates that there has been no significant change in the distribution of Mycobacterium tuberculosis lineages over time. The study revealed that among the selected Mycobacterium tuberculosis strains, resistance rates to first-line anti-tuberculosis drugs were as follows: isoniazid (39%), rifampicin (21%), ethambutol (19%), and streptomycin (34%). Genotypic analysis indicated that the Beijing lineage was predominantly associated with drug-resistant tuberculosis cases, including multidrug-resistant (MDR), poly-drug-resistant, and mono-drug-resistant TB. Notably, the Beijing lineage accounted for 100% of pre-extensively drug-resistant (pre-XDR) TB cases. Within the Haarlem lineage, 33% were MDR-TB. In the Latin American-Mediterranean (LAM) lineage, 13.3% were MDR-TB, 6.6% were poly-drug-resistant, and 13.3% were mono-drug-resistant. Among the mainly T lineage, 42.8% exhibited mono-drug resistance. These findings suggest that the distribution of M. tuberculosis lineages in the Mongolian population has remained relatively stable over time, with no significant temporal changes. Conclusion The distribution of M. tuberculosis genotypes circulating among the population of Mongolia has remained relatively stable over time, with no significant time-dependent changes. Additionally, no mutations associated with resistance to newly introduced anti-TB drugs were detected.

BACKGROUND: Toll like receptors (TLRs) are a class of proteins that key role in the innate immune system. TLR7 is expressed on monocytes, macrophages and dendritic cells, T cell, B cell and eosinophiles. TLR7, originally identified as recognizing imidaquinoline, loxibrine, broprimine and ssRNA, ssRNA viruses such as vesicular stomatitis virus, influenza A virus and human immunodefiency virus. It is known that virus ssRNA affects signaling molecule of IFN-y. Objective: To determine gene and protein activation of IFN-y signal transduction by TLR7 ligand in the endothelial cells. MATERIAL: In study we used mouse aortic linear endothelial cell which is cultured (END-D) in 5% heat- inactivated fetal calf serum (FCS), medium (DMEM) containing antibiotic mix(penicillin G, streptomycin, amphotericin B) at 37°C (5% CO2). Endothelial cells treated with synthetic IFN-γ and imiquimodligands, then the NO (nitric oxide) concentration in the supernatant is determined by Griess reagent. Endothelial cells are cultured in 6 well cell culture plate and in each well 2*104cells are expected to be grown for 24 hours of culture. Then, the cells are treated with synthetic IFN-γ and имиквимод ligand for 6 hours and the NO signaling gene activation iNOS mRNA expression which is induced by IFN-γ is determined by RT-qPCR. Endothelial cells are cultured in 12 well cell culture plate and in each well 2*104 cells are expected to be grown for 18 hours of culture. Then, the cells are treated with synthetic IFN-γ and imiquimodligands for 24 hours and the NO signaling protein iNOS expression which is induced by IFN-γ is determined by western blotting. The experiment was conducted as representation mean of at least three test results. The difference between statistical probabilities is determined by the “Students” t test. The p<0.01 value is assumed to be statistically different. RESULTS: TLR7 ligand imiquimodaugmented interferon gamma induced nitric oxide production TLR7 ligand imiquimodincreased interferon gamma induced iNOS mRNA gene expression. TLR7 ilgand imiquimodup-regulated interferon gamma induced iNOS protein expression. CONCLUSIONS: TLR7 ligand imiquimod augments IFN-γ signaling in the endothelial cells. This synergistic effect has revealed in the levels of gene and protein expression.

Introduction: The aim of this research project is to elucidate the crosstalk of innate and adaptive immune reactions against the DNA containing bacteria. : This study held in the Core laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). Murine aortal endothelial cells, END-D cultured and the cell viability checked by MTT assay. In addition, the NO production, protein and gene expression studied by Griess Reagent assay, R.T-PCR and immunoblotting, respectively. Results: 0.1µM, 1µM and 10µM of TLR9 ligand exhibited no cytotoxic action against the cells by MTT assay. IFN-ү alone induced NO production in END-D cells. In the other hand, TLR9 ligand at 0.1µM, 1µM and 10µM up-regulated IFN-ү induced NO production in dose dependent manner. RTPCR results exhibit that TLR9 ligand up regulates iNOS mRNA. Immunoblotting analysis showed the enhanced iNOS protein expression and phosphorylation of STAT1 in cells pre-treated with TLR9 ligand. Discussion: We have demonstrated CpG DNA, TLR9 ligand, up-regulates IFN-ү induced NO via enhanced IFN-ү signaling. The result of Western Blotting and RT-PCR support the up-regulation of NO. CpG DNA can be used as agent against virus and bacteria. Further research need to be conducted. Conclusion TLR9 ligand, CpG DNA up-regulates IFN-ү induced NO production in time and dose dependent manner. TLR9 ligand augments the expression of iNOS mRNA and STAT1 phosphorylation in response to IFN-ү.